This syndrome can be classified according to different variables. For example, classification can be based on the type of compression, in which case a distinction must be made between positional or direct compression and crushing.[11] Another form of classification is based on the location of the injury, which can be found in the head, thorax, abdomen, pelvis or extremities. The syndrome can also be classified by a combination of soft tissue injuries, for example, with damage to internal organs, with damage to bones and joints, and with damage to vessels and nerve trunks. Classification may also be based on the severity of the injuries, which in turn is classified according to the duration of the compression.[11] For example, after four hours of compression the injuries may be mild, when the compression lasts up to six hours they are of moderate severity, and after compression of an entire extremity for a period of seven to eight hours the injuries will be severe and will be associated with characteristic signs of acute renal failure and hemodynamic disorder. An extremely serious form of injury is compression injury to one or both legs with exposure of more than eight hours.[11]​.

According to another author,[12] it is possible that around four hours of compression may be required for a true crush syndrome to appear, although this question has never been formally studied.[12] In another work already mentioned[7]​ it is stated that the duration of the crush period is one of the most critical factors regarding the outcome of victims who survive the first traumatic impact and it is reported that this period has been established as one hour of intense compression or four to six hours of compression moderate.[7]​.

Another classification of injuries and crush syndrome is related to the type of disaster in which they occur. For example, according to one publication,[13] disasters are often classified as "natural" and "man-made" and are sometimes subdivided into "slow-onset" and "sudden-onset," distinctions that are generally useful in terms of their descriptiveness but do not allow satisfactory classification of immediate causes or the effects of different agents. The authors of the aforementioned publication[13]​ use a classification of natural disasters that includes only earthquakes, cyclones and storms, tornadoes, tsunamis, floods and volcanic eruptions. According to them, this delimitation is due to two reasons, namely, firstly, the disasters mentioned are those that cause the most deaths, particularly in developing countries, and secondly, these catastrophes constitute the main objective of international relief organizations. Other accidents, such as snow slides or forest fires, have equally disastrous effects on affected communities, but help remains in the hands of local organizations, such as firefighters and police, and is not easy to include in the descriptive classification of disasters.[13]​.

Trauma (including those caused by crushing or compression of the body or limbs) have existed and affected human beings throughout their historical development. It is also true that this phenomenon has been favored by the settlement of large human groups in geographical regions with a high frequency of natural disasters.[10]​ As noted by various authors, in the case of earthquakes, in a few days as many deaths and injuries are recorded as those caused in the long course of armed conflicts. Prevention and preparation against these disasters remain insufficient. In human history, earthquakes have caused at least four million deaths.[10] Every year, up to eighty-five large earthquakes occur, releasing energy equivalent to fifty atomic bombs with a power similar to those dropped on the Japanese cities of Hiroshima and Nagasaki.[10] The large annual number of people with serious injuries is also due to accidents in mines and underground facilities, collapses of damaged buildings, and industrial and transportation accidents. The significant damage that buildings suffer due to wars, especially when aerial or artillery bombardments are used on cities, causes a large number of wounded and injured people with serious trauma.[13]​.

According to one author,[14]​ it is likely that the first description of muscle necrosis in a comatose patient was that formulated by Larrey, the military surgeon in Napoleon's army, who in 1812 reported cases of Napoleonic soldiers unconscious due to carbon monoxide poisoning who developed skin and muscle necrosis in body areas that had been subjected to static pressure and prolonged immobility.[14]​.

In the German literature, crush syndrome was reported for the first time in 1909 by an author (von Colmers) who described the cases recorded during the earthquake that occurred in Messina (Sicily) in 1908 as "acute pressure necrosis", with the description of a single patient with a change in urine color and oliguria due to the late arrival of the mission.[14] In the German military medical literature there are also reports of cases that occurred during the First War. World.[15]​ Frankenthal (in 1916) was the first to describe cases of traumatic rhabdomyolysis and acute renal failure as a result of war wounds. Several other authors described symptoms of rhabdomyolysis observed in soldiers who had remained buried in the trenches with pressure on their limbs during the fighting and who presented edema and associated muscle necrosis.[10]​.

According to another publication,[16]​ while it is true that the first description of acute renal failure secondary to crush injuries after war injuries and motor vehicle accidents was formulated in the early 20th century, the most detailed description of the syndrome was that made by Bywaters and Beall after the Battle of London, during World War II. However, the first catastrophe of epidemic proportions occurred in the wake of a natural disaster—the 1988 Armenian earthquake. Since then, crush injuries caused by at least eight other mass disasters have resulted in numerous casualties or victims in need of dialysis.[16]​.

In summary, the first descriptions of crush syndrome appeared in the German-language literature after the Messina earthquake of 1909 and the Second World War.[14]​ At the threshold of that war, the syndrome was not yet discussed in the English-language literature and it was not until after the London bombing of 1940 that Bywaters and Beall clearly described the pathogenesis and established guidelines for the management of victims,[3]​ which began the modern history of crush syndromes.[14] Bywaters and Beall reported four cases of crush syndrome whose victims had presented with shock, inflammation of the affected extremities, dark urine, progressive development of kidney failure and finally death. On histological examination of the kidneys there was evidence of tubular necrosis and pigmented casts.[3]​ In 1944 Bywaters and Stead identified myoglobin as the urinary pigment and proposed its main role in the development of renal failure.[12][17][3]​.

Detailed reporting of these disasters is often lacking because it is generally difficult (if not impossible) to obtain sufficient documentation. On some occasions there is clear data, as in the case of a report following the sudden collapse of an eight-story historic building in which eighty percent of the trapped victims died instantly from direct trauma, ten percent survived with minor injuries and in the remaining ten percent the injuries were serious and crush syndrome developed in seven of ten cases.[16] If these percentages are extrapolated to massive disasters with the collapse of hundreds of buildings, it will be seen that Spectacular numbers of crush-related casualties can occur, although the final number and outcome of cases depend on many variables (e.g., the severity, type and timing of the disaster, the geological characteristics, the density of the population, the quality of buildings, the effectiveness of rescue activities, the time victims spent under the rubble, and the health infrastructure of the affected region).[16]

Trauma and sustained muscle compression are common causes of rhabdomyolysis (the traumatic rhabdomyolysis mentioned at the beginning) that can be observed in different situations.[9]​ For example, after some traffic accidents and building collapses, victims of multiple trauma remain trapped for hours, in events that generate large crowds of people (football stadiums, concerts, youth parties) there may be episodes of crushing, prolonged immobilization in comatose subjects generate muscle compression, as do surgical procedures with muscle compressions maintained in a forced position or with the use of tourniquets, some bone fractures, particularly those of the tibia, can cause acute compartment syndromes of the lower extremities and, finally, injuries produced by electricity (lightning, electric shocks) and extensive third-degree burns can also cause rhabdomyolysis.[9]​ In patients with burns caused by electricity or chemical substances, the damage Muscular strength is greater in the tendon insertions and periosteal regions. Massive muscle destruction (rhabdiomyolysis) causes myoglobinemia and precipitation of myoglobin in the renal tubules can produce acute tubular necrosis and renal failure if left untreated.[18]​.

Contenido

El médico japonés Seigo Minami, que informó por primera vez el síndrome de aplastamiento en 1923,[19]​[20]​[21]​ estudió la patología de tres soldados muertos por insuficiencia renal en la Primera Guerra Mundial. Según él, los cambios renales se debían a un infarto causado por la metahemoglobina resultante de la destrucción de los músculos, patología que también se observa en personas enterradas vivas, y la insuficiencia renal aguda progresiva era secundaria a necrosis tubular aguda.[22]​.

Como ya se comentó, el síndrome fue descrito posteriormente por el médico británico Eric Bywaters en cuatro civiles afectados durante el bombardeo de Londres de 1941.[3]​[23]​ Según esa descripción, se trata de una lesión por reperfusión que aparece después de la liberación de la presión de aplastamiento. Se cree que el mecanismo lesional es la liberación en la circulación de los productos de la degradación muscular —en especial mioglobina, potasio y fósforo—, es decir los productos de la rabdomiólisis (la desintegración del músculo esquelético dañado por la isquemia).[3]​ La acción específica sobre los riñones no se entiende bien pero se piensa que puede atribuirse en parte a metabolitos nefrotóxicos de la mioglobina.

Cuando se levanta el hormigón y la circulación se restablece el líquido se precipita en la zona afectada hasta diluir los electrólitos liberados de modo que su concentración en el sitio coincide con la del resto del cuerpo. En circunstancias normales los líquidos corporales circulan a través de dos espacios —los vasos sanguíneos y el interior de las células— pero después de una lesión por aplastamiento o de cualquier condición que agote las reservas de proteínas (p.ej., insuficiencia hepática o desnutrición) el líquido queda secuestrado en un espacio extravascular (que se conoce como "tercer espacio").[24]​ En algunas víctimas de terremotos en un miembro dañado e hinchado podrían llegar a quedar secuestrados varios litros de líquido en los días posteriores al rescate, lo que aumentaría considerablemente la presión en la zona afectada con disminución de la presión arterial en el resto del cuerpo. Para prevenir la hipotensión, que puede dañar rápidamente los órganos vitales, las víctimas de aplastamiento reciben líquidos a través de un goteo intravenoso incluso antes de ser liberadas. Ese líquido adicional puede determinar que la sangre se diluya, con la anemia consiguiente.[24]​.

From crush injuries

The pathophysiology of crush injuries is not completely known, but it is known that for them to occur, intense or prolonged compression is required and that the main injury is that of the muscle.[25]​ The difference between crush injuries and vascular occlusion injuries is that in the former there is no skin necrosis and distal pulses also persist; The difference between crush injuries and injuries due to intense and short-term direct impact consists in the absence of the skin and cellular tissue injury characteristic of the latter.[26]​.

The condition most similar to a crush injury is the compartment syndrome resulting from the elevation of pressure in the muscular compartments that produces occlusion of venous drainage from the compartment, which in turn generates a greater elevation in pressure with the final result of necrosis of the muscle in the affected place.[25] However, although the clinical pictures are similar and were once thought to share the same pathophysiology, that of the crush injury is the opposite because in it the muscle damage is produced by pressure. continuous external pressure and as a result of this damage the muscle cells lose their ability to control fluids and become edematous, which determines the elevation of compartmental pressure.[25]​ Therefore, the elevation of compartmental pressure in crush injury is secondary to muscle damage, and not the cause of it, as in the case of compartment syndrome. As is obvious, in many circumstances both pathogenic mechanisms act together in the same case.[25]​.

Although cellular events that occur during ischemia have long been known to contribute to the pathogenesis of organ injury, the contribution of reperfusion to this process has only recently been recognized. Restoration of blood flow after prolonged ischemia aggravates tissue damage by causing additional injury or by unmasking the injury produced during the ischemic period. This phenomenon is known as ischemia-reperfusion injury.[27]​.

When skeletal muscle undergoes a prolonged period of ischemia, significant necrosis associated with substantial morbidity and mortality from local and systemic complications can occur. Muscle damage occurs both during the period of ischemia and during reperfusion. During the period of ischemia, there is depletion of energy stores as a result of the continuous demands to maintain ionic compartmentalization and other homeostatic processes and the reduced capacity to regenerate adenosine triphosphate (ATP) (adenosine triphosphate) by oxidative phosphorylation. If ischemia lasts long enough, muscle damage becomes irreversible.[27]​

Although necessary for the restoration of metabolic activity, reperfusion increases the magnitude of necrosis and it is likely that much of the muscle damage occurs after the restoration of oxygenation rather than during the period of ischemia, that is, during reperfusion. Many factors are involved in reperfusion injury but today the main causes are considered to be the release of oxygen radicals "Radical (chemistry)"), the massive accumulation of calcium inside muscle cells ischemic events and the infiltration of neutrophils into the reperfused vessels, with consequent occlusion.[28]​.

Regarding the pathogenesis, after an episode of rhabdomyolysis, large amounts of myoglobin are released that are filtered by the glomeruli and then degraded with the release of heme pigment, which is toxic to the kidney.[9] The three injury mechanisms are tubular obstruction in association with uric acid, direct damage to the proximal tubule cells, and vasoconstriction with reduced blood flow. However, other predisposing factors are required because myoglobinuria itself rarely causes kidney damage. Among these factors, volume depletion can be mentioned, which favors vasoconstriction and cylinder deposition.[9]​.

Crush syndrome

Crush syndrome has a pathophysiology so similar to that of rhabdomyolysis that currently crush syndrome is synonymous with traumatic rhabdomyolysis, a common syndrome in which skeletal muscle injury determines the release of myocyte contents into the plasma "Plasma (blood)").[26] Among the numerous factors that can induce rhabdomyolysis is crushing of the extremities. Disruption of tissue perfusion in a muscle group causes crush syndrome. Injury mechanisms may consist of direct muscle trauma, blunt or penetrating trauma, or extended pressure on a muscle mass. Muscle compression is important in the etiology of more than forty percent of patients with traumatic rhabdomyolysis.[26] Microvascular trauma secondary to prolonged application of a compressive force generates hypoperfusion, cellular hypoxia, or both. Hemorrhage from vascular rupture can alter blood flow and oxygen delivery to tissues. Bleeding into an intact compartment can lead to compartment syndrome, which decreases perfusion and produces local neurovascular dysfunction.[26] Hemorrhage, edema, and hypoperfusion combine to produce tissue hypoxia and ischemia. With pressures of only 20 mm Hg, capillary blood flow can be affected with consequent hypoxic damage due to a decrease in oxygen tension. The efflux of damaged muscle products, metabolic changes, and internal volume losses apparently do not begin until after removal and decompression of the extremities. After rescue and extraction of the victims, reestablishment of blood flow to the ischemic extremity allows the perfused fluid to localize to the damaged tissues and cause edema, hemoconcentration, and clinical shock. Since after the extraction of the damaged limb the membrane of the muscle cells loses its ability to control ionic exchange, water enters the cell freely, in addition to calcium and sodium, which determines significant muscle edema that is associated with hypovolemia and shock because the liquid comes primarily from the intravascular space. In addition, the breakdown products of damaged cells (the most important of which are potassium, phosphorus and myoglobin, which is the basic pigment of muscle cells) pass into the bloodstream. Myoglobin released into the plasma is filtered by the glomeruli and appears for a time in the urine as pigmented casts. Volume depletion, together with the release of acidic components by the injured muscle, produces a decrease in urinary pH and due to the low pH myoglobin forms a gel that obstructs the distal nephron and generates oliguria.[26] In addition, the combination of hypovolemia, acidemia and myoglobinemia can produce acute renal failure. The process just described becomes a vicious circle because as the kidney stops eliminating the previous degradation products, the risk of death from hyperkalemia increases. The mechanism of production of renal failure is multiple: the causes of acute renal failure in traumatic rhabdomyolysis include microthrombi in the glomerular capillaries due to hypercoagulability, hypotension and activation of extrarenal vasoconstriction systems with reduction in renal blood flow, formation of intratubular deposits of urate and pigmented casts, iron nephrotoxicity and inactivation of the intrarenal vasodilatory influences of oxide. nitric acid, direct kidney injury due to elevation of the calcium-phosphorus product (CaxP), kidney damage due to muscle breakdown products other than myoglobin and urates and, finally, an acute case of renal failure due to acute hyperphosphatemia.[26]​.

According to the summary of the pathological anatomy of one of the cases described by Bywaters,[3]​ the point of greatest interest was the condition of the patient's kidneys, which were enlarged (weighing 210 and 230 g, respectively), dark red in color and firm, with a very smooth surface and the capsules in tension as a result of cortical swelling. The cut edges everted the cut surfaces, which were wet and glassy due to exudation of serous fluid. Parts of the cortex located midway between the renal pyramids were pale from zonal ischemia. There was no evidence of ascending infection. The bladder was slightly red and contained a few drops of very dense, cloudy urine. The subcutaneous and retroperitoneal tissues oozed serous fluid when sectioned, indicating mild generalized edema. There was marked cyanosis of the internal parts but the skin was pale. No notable changes were observed in other organs or other tissues.[3]​.

On microscopic examination of the kidney the most severe damage was in the convoluted tubules and the loops of Henle. The cytoplasm of the lining epithelium was swollen, ragged, granular, and vacuolated. In some places, devitalized and desquamated individual cells were seen, while those that remained united showed quite frequent mitosis. The discarded cells in various stages of disintegration fused in the lumen with loose collections of eosinophilic debris. In the loops of Henle and the collecting tubules there were numerous cylinders of dense eosinophilic material, most of them dark brown, as if lightly stained with bile or red blood pigment. All of these cylinders seemed to be made of the same substance, although their morphological appearance varied greatly depending on the degree of condensation they had undergone. Some resembled collections of disintegrating erythrocytes; others simulated shreds of fibrin while others condensed into solid hyaline cylinders. They appeared to be composed of dead epithelial cells, thick albumin, and perhaps hyaline material exuding from the tubular lining.[3] Within the tubules it was possible to identify an occasional erythrocyte, but as far as could be determined by histological means, most of the casts were not red cells, although the color of some could be due to hemoglobin. It is likely that they were not of a specific type, such as casts similar to those seen in acute nephritis and other diseases in which there appears to have been extensive tubular reabsorption with the result of poorly concentrated urine. Some of them were surrounded and invaded by leukocytes and in the lower part of the straight tubules, sometimes leukocytes were the predominant component. Here and there, a tubule filled with cylinders was disintegrating and surrounded by inflammatory cells. Stains for iron were negative. There were no fatty changes. The glomeruli did not show any obvious structural change, although the frequent presence of albuminous material in Bowman's capsule suggested that they had not escaped injury. The glomerular networks contained a relatively small amount of blood, but the vessels of the medullary parts were very congested.[3]​.

In other tissues, such as the thyroid, there were signs of incipient activity with greater cell height and many mitoses. The liver tissue was swollen and opaque but without necrosis. In the adrenal tissue there was irregular loss of cortical lipoid. Vacuolization of neuromuscular fibers (bundle of His) was observed in the cardiac tissue. The muscles of the right leg were normal. The amputated leg showed hemorrhage in the popliteal fossa around the artery, which extended along the intermuscular fascial planes. There was no edema beneath the deep fascia but mild superficial edema with petechiae could be observed over the cutaneous pressure areas. There was hemarthrosis of the knee joint, with cracks in the patellar and tibial cartilages, extending downward through the bone of the tibial condyle. Sections of the artery showed no lesion while sections of the muscle (which macroscopically appeared normal) revealed a few (one percent) necrotic fibers, with loss of striation and stainability.[3]​.

The loss of intravascular volume as a result of the combination of hemorrhage and displacement of intracellular fluids causes shock secondary to hypovolemia.[12]​.

In typical cases of crush syndrome, the aforementioned hypovolemia is also related to the absence of fluid intake for hours or days, which is combined with increased losses and the development of third spaces in the affected muscle areas, a phenomenon that is due to the reperfusion of the injured muscle that follows decompression.[9]​ As a result of the release of large amounts of myoglobin, the urine has a color that varies between red and dark brown. However, unlike what happens in massive hemolysis, in myoglobinuria the plasma maintains its normal color. The severity of renal failure secondary to rhabdomyolysis ranges from mild elevations in markers of renal function to the development of anuric renal failure requiring immediate extracorporeal clearance.[9] Factors that determine the degree of renal injury include the previous condition of the kidneys, age, coexisting diseases, duration and intensity of muscle compression, hypovolemia, concomitant sepsis, and peak creatine phosphokinase (CPK) level. reached.[9]​.

As previously emphasized (see introduction), when talking about crush syndrome, reference is made to the systemic manifestations of the crush injury.[26]​ According to various publications, it is possible that the clinical picture observed in the first hours of the syndrome produces the false impression of a minor problem, which can lead to serious consequences since the success in preventing the development of acute renal failure is directly related to the immediate implementation of therapeutic measures.[26]​ The severity of the clinical manifestations is proportional to the amount of injured muscle. The syndrome appears especially when the injury affects the lower extremities, in which the amount of muscle involved is large. The systemic effects of hypovolemia and the direct effects of electrolyte disturbances with the associated release of toxins are cardiotoxic. As a result of the massive displacement of fluids from the extracellular space to the damaged muscle, the intravascular volume is reduced and hypovolemic shock develops, the most common cause of death after crush injury in the first four days.[26]​.

Cardiovascular complications are associated with arrhythmias secondary to hyperkalemia and acidosis and are the second most common cause of death in the early phase of crush trauma.

The development of acute respiratory distress syndrome, one of the most serious complications, can be triggered by the release of inflammatory mediators by injured cells or by direct trauma. The event can also be complicated by fat embolism.

Renal failure is the most serious complication of crush syndrome and its pathogenesis in this syndrome is multifactorial, with the intervention of vasomotor and nephrotoxic elements. As a result of circulatory shock and intravascular volume depletion, vasoconstriction of the afferent arterioles occurs with consequent renal cortical ischemia. Myoglobin, urates, and phosphate released by muscle cells cause precipitation in the distal convoluted tubules and formation of tubular casts with resulting obstruction, all potentiated by urine concentration and acidity secondary to hypovolemia and metabolic acidosis. It has been suggested that myoglobin produces oxidative renal injury as a result of lipid peroxidation induced by myoglobin cycling between oxidized and reduced forms. What is characteristic is that after a few hours after the rescue, when the blood concentrations of urea and creatinine are still within normal limits, a risky degree of hyperkalemia (more than 6 mEq/L), hypokalemia (less than 8 mg/dL), hyperphosphatemia (more than 6 mg/dL), hyperuricemia (more than 8 mg/dL) and metabolic acidosis occurs.

Hemoconcentration, and sometimes thrombocytopenia, may suggest the onset of disseminated intravascular coagulation. It is also characteristic that very high blood levels of CPK (more than 10,000 U/L) and myoglobin are observed. The CPK level, which has been linked to the development of kidney failure and mortality, is the most sensitive indicator of crush syndrome. The first line of defense against hyperkalemia, skeletal muscle, is rapidly disrupted during rhabdomyolysis. The result is a particularly risky fulminant hyperkalemia because cardiotoxicity is enhanced by hypocalcemia and shock. Muscle disruption may be associated with immediate critical hyperkalemia (7 to 9.5 mEq/L). In these cases, cardiac arrest can occur in the hour following removal of the limb.

La conjunción de orina oscura, elevación importante del nivel plasmático de creatinfosfocinasa e insuficiencia renal en un paciente con antecedentes traumáticos establece el diagnóstico.[9]​ Sin embargo, en los pacientes traumatizados existen otras causas de insuficiencia renal, entre ellas la hipovolemia, la sepsis y los fármacos nefrotóxicos que se emplean para tratarlos. En un caso de rabdomiólisis el análisis de orina mostrará positividad para microhematuria en las tiras reactivas habituales (por la presencia de pigmento hemo) con ausencia de eritrocitos en el análisis microscópico de la orina. La concentración sérica de creatinfosfocinasa, que aumenta siempre en los pacientes con rabdomiólisis, llega a valores mil veces más elevados que los normales. El nivel máximo de esa enzima se alcanza alrededor de veinticuatro horas después del daño muscular, con un rápido descenso posterior.[9]​ Existe poca correlación entre los valores máximos de creatinfosfocinasa y los niveles de creatinina. Es raro que se desarrolle una insuficiencia renal aguda cuando el nivel de creatinfosfocinasa no supera las 10 000 unidades internacionales (U/L).

En el terremoto ocurrido en Japón en 1995 (gran terremoto de Hanshin-Awaji) el ochenta y cuatro por ciento de las víctimas con valores de creatinfosfocinasa superiores a 75 000 U/L requirieron diálisis en comparación con el treinta y nueve por ciento de los pacientes que no superaron esa cifra. La liberación del potasio intracelular puede generar una hiperpotasemia grave y hasta desproporcionada con respecto al grado de insuficiencia renal, con elevaciones sostenidas y rápidas a pesar de la ausencia de aportes exógenos.[9]​ Las alteraciones del calcio sérico son frecuentes en el síndrome de aplastamiento.

Al principio suele haber hipocalcemia debida al aumento de los niveles de fósforo y al depósito de fosfato de calcio en el músculo lesionado pero durante la fase de recuperación es más común la hipercalcemia por movilización del calcio que se había depositado en el músculo y la corrección de la hiperfosfatemia que genera una mejoría de la función renal. La detección de niveles elevados de aspartato transaminasa (AST), alanina transaminasa (ALT) y lactato deshidrogenasa (LDH) es frecuente y puede ser el primer hallazgo de laboratorio. En este contexto la elevación del nivel de esas enzimas no debe interpretarse como signo de lesión hepática si no se acompaña de otros datos compatibles con ese diagnóstico.[9]​.

in the field

The presence of myoglobin is suggested by the reddish or dark color of the urine (hematuric urine) and ortholidene test strips (urinalysis strips) are used to detect it locally. The solubility of myoglobin in urine is given by urinary pH and therefore the modification of this variable with medications is one of the treatment modalities. A urinary pH less than 5 (acidic) precipitates more than seventy percent of myoglobin, which quickly leads to kidney failure. A urinary pH greater than 6.5 precipitates less than five percent of myoglobin. A pH above 7.5 prevents precipitation and protects the kidney from imminent failure.

Differential diagnosis can be established with a spinal cord injury due to intact sphincters in cases of entrapment of both lower extremities.[7]​.

Según Michaelson, el objetivo principal del tratamiento de los pacientes con lesiones por aplastamiento debe ser evitar que desarrollen el síndrome homónimo, que se asocia con una tasa elevada de morbilidad y mortalidad.[25]​ Siempre según ese autor, el tratamiento de las extremidades afectadas es objeto de controversias. Todavía hay muchos médicos que creen que la similitud que existe entre los signos de las lesiones por aplastamiento y el síndrome compartimental exige que se los trate de la misma manera,[29]​

es decir con una fasciotomía temprana.[25]​ Sin embargo, ese procedimiento no da buenos resultados y es la causa de las pocas muertes informadas en la bibliografía.[25]​.

El síndrome de aplastamiento es una secuencia predecible de complicaciones que siguen a una lesión por aplastamiento. Las lesiones importantes de los tejidos blandos predisponen a los pacientes a múltiples complicaciones entre las que figuran cambios fisiológicos que incluyen hipovolemia, síndrome compartimental, rabdomiólisis, desequilibrios electrolíticos y ácido-base, coagulopatía e insuficiencia renal. Es fundamental tomar las medidas necesarias para reducir al mínimo las complicaciones mediante una evaluación precisa y la implementación de intervenciones terapéuticas correctas.[30]​.

Amputation

The most drastic response to crushing under fallen structures or other objects may be field amputation. In the description of one of his four cases (case I) Bywaters[3]​ commented that prevention through early amputation had been considered adequate but it was later found that it was evident that thirty-six hours was not early enough. His conclusion was that if there was an alternative that would allow immediate amputation to be avoided, it would only be found with a deeper and more complete investigation of these patients, through careful observation of the effects of the treatment or if the condition could be reproduced in the laboratory and, according to him, studies were already being developed at his institution to induce this state under experimental conditions.[3]​ According to the Emergency Medical Services Agency of the city of San Francisco "San Francisco (California)"),[31]​ if the entrapment is endangering the life of rescuers or the patient, field amputation should be considered. The protocol of that institution indicates that in these cases the incident commander be consulted about possible environmental threats to the rescue and contact be established with the doctor at the base hospital to set up a surgical team at the scene of the amputation.[31]​.

The lingering effects of crush syndrome can be fatal even days or weeks after rescue. According to the author of one publication,[24] in a study of eighteen patients admitted to an intensive care unit after the 1999 earthquake in Marmara (Turkey), it was found that eight of them had not survived their stay in the hospital. In the earthquake that occurred on January 12, 2010 in Haiti, doctors faced a particularly difficult situation because although crush syndrome can be managed by strictly monitoring electrolyte levels, in Haiti medical centers had been destroyed by the earthquake, modern equipment was scarce, and electricity was difficult to obtain. Therefore amputation, whether in the field or in an operating room, was often the safest option.[24]​.

The author of this work on the earthquake that affected the population of Haiti in January 2010 wonders if it is possible to die from the crushing of a limb and, obviously, his answer is affirmative.[24] If compression of an arm or leg occurs for less than four hours (a period that is reduced to two hours if it is an elderly person or a person with circulatory problems) there is a good chance that the doctor will be able to save the life and limb of the person. affected person.[24]​ On the other hand, if a person with a limb compressed for more than eight hours survives (because they do not have an open fracture or have succumbed to blood loss) they will most likely require amputation but will otherwise do well. Between these two periods, the decision that doctors must make is difficult because they may try to save a victim's arm or leg but the toxins released by the damaged tissues could enter the circulation, which would imply a high risk of multiple organ failure.[24]​.

During the first phase of crush syndrome the limb is still trapped under concrete or other material structures and therefore without blood flow in any direction. As a result, muscle tissue begins to die and collapsed cells release proteins, potassium, and lactic acid.[24] Those chemicals, which under normal circumstances circulate through the body in much lower concentrations, accumulate in the affected area. Dead muscles also tend to stiffen and if the compressed limb shows a wood-like consistency similar to rigor mortis, it will most likely need to be amputated.[24]​.

Finally, according to specialists in this syndrome, although it is feasible to completely extract a patient in stages, adequate physiological preparation is mandatory: in crush syndrome the conventional procedures for prehospital care are fluid replacement and permissive hypotension.[32][33]​.

Permissive hypotension

The term permissive hypotension refers to the therapeutic procedure implemented in patients with active hemorrhage before surgical control without modifying the systolic blood pressure (SBP) (which is maintained between 80 and 90 mm Hg) with the purpose of sustaining tissue perfusion without exacerbating hemorrhage. The scientific bases of this therapeutic modality are found in experimental studies in which it was demonstrated that attempts to achieve normal values ​​of systemic blood pressure before achieving control of hemorrhage are associated with the risk of increased blood loss and mortality.[32][33]​.

According to another publication, hypotensive resuscitation (or permissive hypotension) in the context of traumatic injuries can be defined as the deliberate decision to allow blood pressure to remain below normal until any active bleeding has been controlled.[34]​.

The dangers of aggressive fluid resuscitation of trauma patients were recognized as early as World War I, but until recently this type of resuscitation was the mainstay of trauma management. Aggressive resuscitation of the polytraumatized patient is based on animal studies in the 1950s and 1960s, studies that used models of controlled hemorrhage instead of uncontrolled hemorrhage.[34] Consequently, any hypotensive polytraumatized patient was synonymous with aggressive fluid resuscitation until reaching normotension before reaching surgery, which determined that preoperative mortality from trauma did not improve and that it was anemia. acute caused by bleeding the reason for the fatal outcome.[35]​ The physiological response of the body consists of stopping the hemorrhage and trying to maintain blood flow to the vital organs while aggressive resuscitation increases bleeding because it prevents this response and ruptures the immature clot formed, which increases mortality.[35]​ Most of the studies carried out in animals and the few carried out in humans have shown that hypotensive resuscitation, which consists of infusing fluids only until If the patient has central pulses (systolic blood pressure between 60 and 70 mm Hg), it allows more patients to reach the operating room alive so that bleeding is controlled and wounds are corrected, a fundamental objective of the traumatized patient who is hypotensive.[35]​.

Mortality and the risk of renal failure are higher in patients with CPK values ​​greater than 75,000 U/L.[36]​ According to the same publication,[36]​ the number of compressed limbs allows immediate estimation of the severity of the syndrome. The authors of the publication just mentioned[36]​ demonstrated that crushing of a limb is related to CPK levels of around 50,000 U/L, a value that reflects the extent of underlying muscle damage.

Crushing of one, two, or three limbs is associated with a fifty, seventy-five, and one hundred percent incidence of kidney failure, respectively. On the other hand, it has been found that the combination of an age greater than fifty-five years, an ISS (Injury Severity Score) greater than sixteen, and a CPK value greater than five thousand is associated with a probability of kidney failure of forty-one percent, compared to a probability of three percent if none of these three risk factors exist.[26]​.

The causes of death of patients with crush syndrome without adequate treatment can be divided into immediate and late. Immediate causes include severe head trauma, traumatic asphyxia, early thoracic injuries, hyperkalemia, and hypovolemic shock. The late ones are kidney failure, coagulopathy, hemorrhage and sepsis.[26]​.

The morbidity and mortality rates of crush injuries are high but there is little data on the functional evolution of the extremities affected by this type of injury.[26] Experience in the functional recovery of the extremities is good, particularly in patients who do not undergo a fasciotomy, and despite the wide variety of injuries to which the kidneys of people with crush syndrome are exposed, chronic renal failure has not been described as a complication of acute renal failure in rhabdomyolysis. traumatic.[26]​.

Crush syndrome, as already mentioned, is the systemic manifestation of rhabdomyolysis caused by continuous and prolonged compression of muscle tissue, that is, a reperfusion injury resulting from traumatic rhabdomyolysis. According to one publication,[37] this syndrome can be prevented and treated if medical personnel take into account that patients with crush injuries often present few signs and symptoms and therefore maintain a high index of suspicion during treatment. According to the same author[37]​ the obstacles that must be avoided to respond correctly to a disaster, for example the collapse of a building, are the lack of planning of evacuation routes before the event occurs, the lack of knowledge about who commands the rescue operations in the disaster area, the delay in the treatment of victims after their extraction from the rubble, the delay in the administration of intravenous fluids, a low index of suspicion in cases of injury due to crushing and discontinuation of monitoring of patients at high risk of acute renal failure, among others.[37] A slow and progressive restoration of blood circulation to the compressed region once it is released is recommended, particularly if the crush lasted for several hours. To prevent toxic substances released by the damaged muscle from suddenly entering the general circulation, a compressive bandage on the affected limb or region and a proximal tourniquet, which will be loosened frequently, are recommended. The compressive bandages and tourniquet will be applied immediately after decompression, without allowing any delay.[37]​.

Despite the publication of a detailed description of the clinical picture of four cases of crushing by Bywaters and Beall in 1941,[3] disaster-related crush syndrome went unnoticed until one of the deadliest earthquakes of all time, the Tangshan earthquake of 1976.[5] That earthquake killed 240,000 people and injured 165,000 and In the context of that catastrophe, three important observations were made, namely, the incidence of crush syndrome varied from two to five percent among injured victims, patients with crush injuries, whose general condition appears satisfactory, can die suddenly due to hyperkalemia and finally, regardless of the severity of muscle compression, any patient can develop crush syndrome; Therefore, all cases of crushing should be closely observed for any incipient signs of acute renal failure.[38]​ Those observations were confirmed by several subsequent earthquakes.[39]​[40][41]​.

In 1979 and 1982, respectively, two interesting events were observed that had a great impact on the subsequent therapeutic attitude towards disaster-related crush syndrome. In 1979, seven victims trapped after the total collapse of a building were extracted from the rubble after twelve hours and received the first post-rescue intravenous infusion with a delay of six hours. All of these patients developed acute renal failure within the first day after rescue despite having received volume replacement of between five and ten liters of saline per day.[42] By contrast, in 1982, in a similar incident, of eight patients who were trapped under the rubble of a building, seven began receiving intravenous fluids immediately—even before complete removal—at the site of the collapse. Within two hours of their release, these patients were transferred to a hospital where forced volume replacement treatment with alkaline solutions was continued. None of them developed acute renal failure. The remaining patient, who had been buried under rubble for five and a half hours, once freed was transported to a trauma center after a twenty-four hour delay and until then had only received two liters of intravenous fluid. Upon arrival at the center, this patient had already developed established acute renal failure, the treatment of which required supportive dialysis for a month.[43] These observations underscore the vital importance of crush victims receiving fluid replacement as soon as possible, if possible before extraction.[5]

The concepts "renal disaster", "seismonephrology" and "disaster nephrology" have evolved.[5] During the 1988 Armenian earthquake, which caused around 150,000 deaths, rescue teams arrived at the disaster zone with considerable delay and found that about six hundred victims who had been rescued from the rubble after the fact had developed acute kidney failure, after which many of them had died from lack of dialysis.[44]​ In fact, that event was the origin of the term "renal disaster." The extensive support that Armenia received from abroad was of little use[45]​ because at that time there was no organized international support structure available.[46]​ Later the International Society of Nephrology founded the organization called Renal Disaster Relief Task Force (RDRTF),[note 2]​ a global body of kidney experts whose volunteers (doctors and nurses) provided their help for the first time in the 1999 İzmit Earthquake in Turkey, where four hundred and sixty-two people received dialysis with positive results.

Of the six hundred and thirty-nine patients with crush syndrome recorded in the 1999 Marmara earthquake, four hundred and seventy-seven required dialysis support and more than five thousand dialysis treatments were applied.[49] Among all subsequent well-documented earthquakes the largest number of patients with acute renal failure related to crush injuries was reported after the Kobe disaster in Japan in 1995, with two hundred and two cases.[36]

According to an already mentioned publication,[43]​ to prevent systemic complications in patients with crush injuries, aggressive fluid treatment should be administered. Furthermore, the authors of the work clarify that to achieve this purpose it is not necessary to excise dead muscle.[43] On the other hand, according to them, an open crush injury requires fasciotomy and immediate radical debridement of the dead muscle tissue and may also require amputation through healthy tissue in an extremity with significant skin laceration. Finally, the same publication advises that a closed crush injury should not be treated surgically until there is demarcation of a gangrenous portion. Even obvious extensive myonecrosis is not an indication for immediate surgical treatment. The only exception to this precept is the need to perform a fasciotomy to save the distal part of the limb if there are no distal pulses or capillary refill and the fasciotomy must be accompanied by radical debridement.[43]​.

Another author[50]​ maintains that the hospital management of crush injuries is essentially that of rabomiolysis. Surgical management is similar to that adopted in all trauma cases. According to him, very aggressive fluid resuscitation, diuresis with fasciotomies when indicated, and monitoring of enzymes and electrolytes will save many limbs and many lives.[50]​.

According to a 2004 publication already mentioned,[41]​ the first objective that should be pursued in the care of disaster victims is to prevent the development of crush syndrome, which can best be achieved through early and massive fluid administration.[41]​ Acute kidney failure resulting from rhabdomyolysis is a major cause of morbidity and mortality in victims rescued from disasters, so its prevention is vital to reduce the number of deaths.[41]​ Since Hypovolemia is the most important factor in the pathogenesis, early and vigorous fluid resuscitation is the most useful therapeutic measure in the prophylaxis of this disorder.[51]​[52]​ The effectiveness of this approach was first demonstrated in victims of crush injuries during a building collapse[42]​ and was subsequently confirmed in victims of the Kobe earthquake, Japan,[41]​ and in a pediatric subgroup of the Marmara earthquake, Turkey.[53]​ However, extensive and uncontrolled fluid resuscitation can cause hypervolemia and related complications, especially in elderly patients and in those in whom treatment is significantly delayed.[51]​ Therefore, fluid resuscitation must be individualized taking into account various medical and logistical variables, namely demographic characteristics, scale of the disaster, environmental conditions, time spent under debris, length of the extraction procedure, volume status and diuresis.[51]​ Because crush syndrome can be avoided with aggressive fluid management,[41]​ patients with crush injury should never be left without treatment, even when dialysis is not available.[54][55]​.

Finally, the best preventive measure to reduce the number of victims of a disaster is to build high-quality buildings. In some cases fixing furniture to walls can also be useful. In the absence of such measures the incidence of disaster-related crush injuries will remain high.[40]​[56]​.

This syndrome can be classified according to different variables. For example, classification can be based on the type of compression, in which case a distinction must be made between positional or direct compression and crushing.[11] Another form of classification is based on the location of the injury, which can be found in the head, thorax, abdomen, pelvis or extremities. The syndrome can also be classified by a combination of soft tissue injuries, for example, with damage to internal organs, with damage to bones and joints, and with damage to vessels and nerve trunks. Classification may also be based on the severity of the injuries, which in turn is classified according to the duration of the compression.[11] For example, after four hours of compression the injuries may be mild, when the compression lasts up to six hours they are of moderate severity, and after compression of an entire extremity for a period of seven to eight hours the injuries will be severe and will be associated with characteristic signs of acute renal failure and hemodynamic disorder. An extremely serious form of injury is compression injury to one or both legs with exposure of more than eight hours.[11]​.

According to another author,[12] it is possible that around four hours of compression may be required for a true crush syndrome to appear, although this question has never been formally studied.[12] In another work already mentioned[7]​ it is stated that the duration of the crush period is one of the most critical factors regarding the outcome of victims who survive the first traumatic impact and it is reported that this period has been established as one hour of intense compression or four to six hours of compression moderate.[7]​.

Another classification of injuries and crush syndrome is related to the type of disaster in which they occur. For example, according to one publication,[13] disasters are often classified as "natural" and "man-made" and are sometimes subdivided into "slow-onset" and "sudden-onset," distinctions that are generally useful in terms of their descriptiveness but do not allow satisfactory classification of immediate causes or the effects of different agents. The authors of the aforementioned publication[13]​ use a classification of natural disasters that includes only earthquakes, cyclones and storms, tornadoes, tsunamis, floods and volcanic eruptions. According to them, this delimitation is due to two reasons, namely, firstly, the disasters mentioned are those that cause the most deaths, particularly in developing countries, and secondly, these catastrophes constitute the main objective of international relief organizations. Other accidents, such as snow slides or forest fires, have equally disastrous effects on affected communities, but help remains in the hands of local organizations, such as firefighters and police, and is not easy to include in the descriptive classification of disasters.[13]​.

Trauma (including those caused by crushing or compression of the body or limbs) have existed and affected human beings throughout their historical development. It is also true that this phenomenon has been favored by the settlement of large human groups in geographical regions with a high frequency of natural disasters.[10]​ As noted by various authors, in the case of earthquakes, in a few days as many deaths and injuries are recorded as those caused in the long course of armed conflicts. Prevention and preparation against these disasters remain insufficient. In human history, earthquakes have caused at least four million deaths.[10] Every year, up to eighty-five large earthquakes occur, releasing energy equivalent to fifty atomic bombs with a power similar to those dropped on the Japanese cities of Hiroshima and Nagasaki.[10] The large annual number of people with serious injuries is also due to accidents in mines and underground facilities, collapses of damaged buildings, and industrial and transportation accidents. The significant damage that buildings suffer due to wars, especially when aerial or artillery bombardments are used on cities, causes a large number of wounded and injured people with serious trauma.[13]​.

According to one author,[14]​ it is likely that the first description of muscle necrosis in a comatose patient was that formulated by Larrey, the military surgeon in Napoleon's army, who in 1812 reported cases of Napoleonic soldiers unconscious due to carbon monoxide poisoning who developed skin and muscle necrosis in body areas that had been subjected to static pressure and prolonged immobility.[14]​.

In the German literature, crush syndrome was reported for the first time in 1909 by an author (von Colmers) who described the cases recorded during the earthquake that occurred in Messina (Sicily) in 1908 as "acute pressure necrosis", with the description of a single patient with a change in urine color and oliguria due to the late arrival of the mission.[14] In the German military medical literature there are also reports of cases that occurred during the First War. World.[15]​ Frankenthal (in 1916) was the first to describe cases of traumatic rhabdomyolysis and acute renal failure as a result of war wounds. Several other authors described symptoms of rhabdomyolysis observed in soldiers who had remained buried in the trenches with pressure on their limbs during the fighting and who presented edema and associated muscle necrosis.[10]​.

According to another publication,[16]​ while it is true that the first description of acute renal failure secondary to crush injuries after war injuries and motor vehicle accidents was formulated in the early 20th century, the most detailed description of the syndrome was that made by Bywaters and Beall after the Battle of London, during World War II. However, the first catastrophe of epidemic proportions occurred in the wake of a natural disaster—the 1988 Armenian earthquake. Since then, crush injuries caused by at least eight other mass disasters have resulted in numerous casualties or victims in need of dialysis.[16]​.

In summary, the first descriptions of crush syndrome appeared in the German-language literature after the Messina earthquake of 1909 and the Second World War.[14]​ At the threshold of that war, the syndrome was not yet discussed in the English-language literature and it was not until after the London bombing of 1940 that Bywaters and Beall clearly described the pathogenesis and established guidelines for the management of victims,[3]​ which began the modern history of crush syndromes.[14] Bywaters and Beall reported four cases of crush syndrome whose victims had presented with shock, inflammation of the affected extremities, dark urine, progressive development of kidney failure and finally death. On histological examination of the kidneys there was evidence of tubular necrosis and pigmented casts.[3]​ In 1944 Bywaters and Stead identified myoglobin as the urinary pigment and proposed its main role in the development of renal failure.[12][17][3]​.

Detailed reporting of these disasters is often lacking because it is generally difficult (if not impossible) to obtain sufficient documentation. On some occasions there is clear data, as in the case of a report following the sudden collapse of an eight-story historic building in which eighty percent of the trapped victims died instantly from direct trauma, ten percent survived with minor injuries and in the remaining ten percent the injuries were serious and crush syndrome developed in seven of ten cases.[16] If these percentages are extrapolated to massive disasters with the collapse of hundreds of buildings, it will be seen that Spectacular numbers of crush-related casualties can occur, although the final number and outcome of cases depend on many variables (e.g., the severity, type and timing of the disaster, the geological characteristics, the density of the population, the quality of buildings, the effectiveness of rescue activities, the time victims spent under the rubble, and the health infrastructure of the affected region).[16]

Trauma and sustained muscle compression are common causes of rhabdomyolysis (the traumatic rhabdomyolysis mentioned at the beginning) that can be observed in different situations.[9]​ For example, after some traffic accidents and building collapses, victims of multiple trauma remain trapped for hours, in events that generate large crowds of people (football stadiums, concerts, youth parties) there may be episodes of crushing, prolonged immobilization in comatose subjects generate muscle compression, as do surgical procedures with muscle compressions maintained in a forced position or with the use of tourniquets, some bone fractures, particularly those of the tibia, can cause acute compartment syndromes of the lower extremities and, finally, injuries produced by electricity (lightning, electric shocks) and extensive third-degree burns can also cause rhabdomyolysis.[9]​ In patients with burns caused by electricity or chemical substances, the damage Muscular strength is greater in the tendon insertions and periosteal regions. Massive muscle destruction (rhabdiomyolysis) causes myoglobinemia and precipitation of myoglobin in the renal tubules can produce acute tubular necrosis and renal failure if left untreated.[18]​.

Contenido

El médico japonés Seigo Minami, que informó por primera vez el síndrome de aplastamiento en 1923,[19]​[20]​[21]​ estudió la patología de tres soldados muertos por insuficiencia renal en la Primera Guerra Mundial. Según él, los cambios renales se debían a un infarto causado por la metahemoglobina resultante de la destrucción de los músculos, patología que también se observa en personas enterradas vivas, y la insuficiencia renal aguda progresiva era secundaria a necrosis tubular aguda.[22]​.

Como ya se comentó, el síndrome fue descrito posteriormente por el médico británico Eric Bywaters en cuatro civiles afectados durante el bombardeo de Londres de 1941.[3]​[23]​ Según esa descripción, se trata de una lesión por reperfusión que aparece después de la liberación de la presión de aplastamiento. Se cree que el mecanismo lesional es la liberación en la circulación de los productos de la degradación muscular —en especial mioglobina, potasio y fósforo—, es decir los productos de la rabdomiólisis (la desintegración del músculo esquelético dañado por la isquemia).[3]​ La acción específica sobre los riñones no se entiende bien pero se piensa que puede atribuirse en parte a metabolitos nefrotóxicos de la mioglobina.

Cuando se levanta el hormigón y la circulación se restablece el líquido se precipita en la zona afectada hasta diluir los electrólitos liberados de modo que su concentración en el sitio coincide con la del resto del cuerpo. En circunstancias normales los líquidos corporales circulan a través de dos espacios —los vasos sanguíneos y el interior de las células— pero después de una lesión por aplastamiento o de cualquier condición que agote las reservas de proteínas (p.ej., insuficiencia hepática o desnutrición) el líquido queda secuestrado en un espacio extravascular (que se conoce como "tercer espacio").[24]​ En algunas víctimas de terremotos en un miembro dañado e hinchado podrían llegar a quedar secuestrados varios litros de líquido en los días posteriores al rescate, lo que aumentaría considerablemente la presión en la zona afectada con disminución de la presión arterial en el resto del cuerpo. Para prevenir la hipotensión, que puede dañar rápidamente los órganos vitales, las víctimas de aplastamiento reciben líquidos a través de un goteo intravenoso incluso antes de ser liberadas. Ese líquido adicional puede determinar que la sangre se diluya, con la anemia consiguiente.[24]​.

From crush injuries

The pathophysiology of crush injuries is not completely known, but it is known that for them to occur, intense or prolonged compression is required and that the main injury is that of the muscle.[25]​ The difference between crush injuries and vascular occlusion injuries is that in the former there is no skin necrosis and distal pulses also persist; The difference between crush injuries and injuries due to intense and short-term direct impact consists in the absence of the skin and cellular tissue injury characteristic of the latter.[26]​.

The condition most similar to a crush injury is the compartment syndrome resulting from the elevation of pressure in the muscular compartments that produces occlusion of venous drainage from the compartment, which in turn generates a greater elevation in pressure with the final result of necrosis of the muscle in the affected place.[25] However, although the clinical pictures are similar and were once thought to share the same pathophysiology, that of the crush injury is the opposite because in it the muscle damage is produced by pressure. continuous external pressure and as a result of this damage the muscle cells lose their ability to control fluids and become edematous, which determines the elevation of compartmental pressure.[25]​ Therefore, the elevation of compartmental pressure in crush injury is secondary to muscle damage, and not the cause of it, as in the case of compartment syndrome. As is obvious, in many circumstances both pathogenic mechanisms act together in the same case.[25]​.

Although cellular events that occur during ischemia have long been known to contribute to the pathogenesis of organ injury, the contribution of reperfusion to this process has only recently been recognized. Restoration of blood flow after prolonged ischemia aggravates tissue damage by causing additional injury or by unmasking the injury produced during the ischemic period. This phenomenon is known as ischemia-reperfusion injury.[27]​.

When skeletal muscle undergoes a prolonged period of ischemia, significant necrosis associated with substantial morbidity and mortality from local and systemic complications can occur. Muscle damage occurs both during the period of ischemia and during reperfusion. During the period of ischemia, there is depletion of energy stores as a result of the continuous demands to maintain ionic compartmentalization and other homeostatic processes and the reduced capacity to regenerate adenosine triphosphate (ATP) (adenosine triphosphate) by oxidative phosphorylation. If ischemia lasts long enough, muscle damage becomes irreversible.[27]​

Although necessary for the restoration of metabolic activity, reperfusion increases the magnitude of necrosis and it is likely that much of the muscle damage occurs after the restoration of oxygenation rather than during the period of ischemia, that is, during reperfusion. Many factors are involved in reperfusion injury but today the main causes are considered to be the release of oxygen radicals "Radical (chemistry)"), the massive accumulation of calcium inside muscle cells ischemic events and the infiltration of neutrophils into the reperfused vessels, with consequent occlusion.[28]​.

Regarding the pathogenesis, after an episode of rhabdomyolysis, large amounts of myoglobin are released that are filtered by the glomeruli and then degraded with the release of heme pigment, which is toxic to the kidney.[9] The three injury mechanisms are tubular obstruction in association with uric acid, direct damage to the proximal tubule cells, and vasoconstriction with reduced blood flow. However, other predisposing factors are required because myoglobinuria itself rarely causes kidney damage. Among these factors, volume depletion can be mentioned, which favors vasoconstriction and cylinder deposition.[9]​.

Crush syndrome

Crush syndrome has a pathophysiology so similar to that of rhabdomyolysis that currently crush syndrome is synonymous with traumatic rhabdomyolysis, a common syndrome in which skeletal muscle injury determines the release of myocyte contents into the plasma "Plasma (blood)").[26] Among the numerous factors that can induce rhabdomyolysis is crushing of the extremities. Disruption of tissue perfusion in a muscle group causes crush syndrome. Injury mechanisms may consist of direct muscle trauma, blunt or penetrating trauma, or extended pressure on a muscle mass. Muscle compression is important in the etiology of more than forty percent of patients with traumatic rhabdomyolysis.[26] Microvascular trauma secondary to prolonged application of a compressive force generates hypoperfusion, cellular hypoxia, or both. Hemorrhage from vascular rupture can alter blood flow and oxygen delivery to tissues. Bleeding into an intact compartment can lead to compartment syndrome, which decreases perfusion and produces local neurovascular dysfunction.[26] Hemorrhage, edema, and hypoperfusion combine to produce tissue hypoxia and ischemia. With pressures of only 20 mm Hg, capillary blood flow can be affected with consequent hypoxic damage due to a decrease in oxygen tension. The efflux of damaged muscle products, metabolic changes, and internal volume losses apparently do not begin until after removal and decompression of the extremities. After rescue and extraction of the victims, reestablishment of blood flow to the ischemic extremity allows the perfused fluid to localize to the damaged tissues and cause edema, hemoconcentration, and clinical shock. Since after the extraction of the damaged limb the membrane of the muscle cells loses its ability to control ionic exchange, water enters the cell freely, in addition to calcium and sodium, which determines significant muscle edema that is associated with hypovolemia and shock because the liquid comes primarily from the intravascular space. In addition, the breakdown products of damaged cells (the most important of which are potassium, phosphorus and myoglobin, which is the basic pigment of muscle cells) pass into the bloodstream. Myoglobin released into the plasma is filtered by the glomeruli and appears for a time in the urine as pigmented casts. Volume depletion, together with the release of acidic components by the injured muscle, produces a decrease in urinary pH and due to the low pH myoglobin forms a gel that obstructs the distal nephron and generates oliguria.[26] In addition, the combination of hypovolemia, acidemia and myoglobinemia can produce acute renal failure. The process just described becomes a vicious circle because as the kidney stops eliminating the previous degradation products, the risk of death from hyperkalemia increases. The mechanism of production of renal failure is multiple: the causes of acute renal failure in traumatic rhabdomyolysis include microthrombi in the glomerular capillaries due to hypercoagulability, hypotension and activation of extrarenal vasoconstriction systems with reduction in renal blood flow, formation of intratubular deposits of urate and pigmented casts, iron nephrotoxicity and inactivation of the intrarenal vasodilatory influences of oxide. nitric acid, direct kidney injury due to elevation of the calcium-phosphorus product (CaxP), kidney damage due to muscle breakdown products other than myoglobin and urates and, finally, an acute case of renal failure due to acute hyperphosphatemia.[26]​.

According to the summary of the pathological anatomy of one of the cases described by Bywaters,[3]​ the point of greatest interest was the condition of the patient's kidneys, which were enlarged (weighing 210 and 230 g, respectively), dark red in color and firm, with a very smooth surface and the capsules in tension as a result of cortical swelling. The cut edges everted the cut surfaces, which were wet and glassy due to exudation of serous fluid. Parts of the cortex located midway between the renal pyramids were pale from zonal ischemia. There was no evidence of ascending infection. The bladder was slightly red and contained a few drops of very dense, cloudy urine. The subcutaneous and retroperitoneal tissues oozed serous fluid when sectioned, indicating mild generalized edema. There was marked cyanosis of the internal parts but the skin was pale. No notable changes were observed in other organs or other tissues.[3]​.

On microscopic examination of the kidney the most severe damage was in the convoluted tubules and the loops of Henle. The cytoplasm of the lining epithelium was swollen, ragged, granular, and vacuolated. In some places, devitalized and desquamated individual cells were seen, while those that remained united showed quite frequent mitosis. The discarded cells in various stages of disintegration fused in the lumen with loose collections of eosinophilic debris. In the loops of Henle and the collecting tubules there were numerous cylinders of dense eosinophilic material, most of them dark brown, as if lightly stained with bile or red blood pigment. All of these cylinders seemed to be made of the same substance, although their morphological appearance varied greatly depending on the degree of condensation they had undergone. Some resembled collections of disintegrating erythrocytes; others simulated shreds of fibrin while others condensed into solid hyaline cylinders. They appeared to be composed of dead epithelial cells, thick albumin, and perhaps hyaline material exuding from the tubular lining.[3] Within the tubules it was possible to identify an occasional erythrocyte, but as far as could be determined by histological means, most of the casts were not red cells, although the color of some could be due to hemoglobin. It is likely that they were not of a specific type, such as casts similar to those seen in acute nephritis and other diseases in which there appears to have been extensive tubular reabsorption with the result of poorly concentrated urine. Some of them were surrounded and invaded by leukocytes and in the lower part of the straight tubules, sometimes leukocytes were the predominant component. Here and there, a tubule filled with cylinders was disintegrating and surrounded by inflammatory cells. Stains for iron were negative. There were no fatty changes. The glomeruli did not show any obvious structural change, although the frequent presence of albuminous material in Bowman's capsule suggested that they had not escaped injury. The glomerular networks contained a relatively small amount of blood, but the vessels of the medullary parts were very congested.[3]​.

In other tissues, such as the thyroid, there were signs of incipient activity with greater cell height and many mitoses. The liver tissue was swollen and opaque but without necrosis. In the adrenal tissue there was irregular loss of cortical lipoid. Vacuolization of neuromuscular fibers (bundle of His) was observed in the cardiac tissue. The muscles of the right leg were normal. The amputated leg showed hemorrhage in the popliteal fossa around the artery, which extended along the intermuscular fascial planes. There was no edema beneath the deep fascia but mild superficial edema with petechiae could be observed over the cutaneous pressure areas. There was hemarthrosis of the knee joint, with cracks in the patellar and tibial cartilages, extending downward through the bone of the tibial condyle. Sections of the artery showed no lesion while sections of the muscle (which macroscopically appeared normal) revealed a few (one percent) necrotic fibers, with loss of striation and stainability.[3]​.

The loss of intravascular volume as a result of the combination of hemorrhage and displacement of intracellular fluids causes shock secondary to hypovolemia.[12]​.

In typical cases of crush syndrome, the aforementioned hypovolemia is also related to the absence of fluid intake for hours or days, which is combined with increased losses and the development of third spaces in the affected muscle areas, a phenomenon that is due to the reperfusion of the injured muscle that follows decompression.[9]​ As a result of the release of large amounts of myoglobin, the urine has a color that varies between red and dark brown. However, unlike what happens in massive hemolysis, in myoglobinuria the plasma maintains its normal color. The severity of renal failure secondary to rhabdomyolysis ranges from mild elevations in markers of renal function to the development of anuric renal failure requiring immediate extracorporeal clearance.[9] Factors that determine the degree of renal injury include the previous condition of the kidneys, age, coexisting diseases, duration and intensity of muscle compression, hypovolemia, concomitant sepsis, and peak creatine phosphokinase (CPK) level. reached.[9]​.

As previously emphasized (see introduction), when talking about crush syndrome, reference is made to the systemic manifestations of the crush injury.[26]​ According to various publications, it is possible that the clinical picture observed in the first hours of the syndrome produces the false impression of a minor problem, which can lead to serious consequences since the success in preventing the development of acute renal failure is directly related to the immediate implementation of therapeutic measures.[26]​ The severity of the clinical manifestations is proportional to the amount of injured muscle. The syndrome appears especially when the injury affects the lower extremities, in which the amount of muscle involved is large. The systemic effects of hypovolemia and the direct effects of electrolyte disturbances with the associated release of toxins are cardiotoxic. As a result of the massive displacement of fluids from the extracellular space to the damaged muscle, the intravascular volume is reduced and hypovolemic shock develops, the most common cause of death after crush injury in the first four days.[26]​.

Cardiovascular complications are associated with arrhythmias secondary to hyperkalemia and acidosis and are the second most common cause of death in the early phase of crush trauma.

The development of acute respiratory distress syndrome, one of the most serious complications, can be triggered by the release of inflammatory mediators by injured cells or by direct trauma. The event can also be complicated by fat embolism.

Renal failure is the most serious complication of crush syndrome and its pathogenesis in this syndrome is multifactorial, with the intervention of vasomotor and nephrotoxic elements. As a result of circulatory shock and intravascular volume depletion, vasoconstriction of the afferent arterioles occurs with consequent renal cortical ischemia. Myoglobin, urates, and phosphate released by muscle cells cause precipitation in the distal convoluted tubules and formation of tubular casts with resulting obstruction, all potentiated by urine concentration and acidity secondary to hypovolemia and metabolic acidosis. It has been suggested that myoglobin produces oxidative renal injury as a result of lipid peroxidation induced by myoglobin cycling between oxidized and reduced forms. What is characteristic is that after a few hours after the rescue, when the blood concentrations of urea and creatinine are still within normal limits, a risky degree of hyperkalemia (more than 6 mEq/L), hypokalemia (less than 8 mg/dL), hyperphosphatemia (more than 6 mg/dL), hyperuricemia (more than 8 mg/dL) and metabolic acidosis occurs.

Hemoconcentration, and sometimes thrombocytopenia, may suggest the onset of disseminated intravascular coagulation. It is also characteristic that very high blood levels of CPK (more than 10,000 U/L) and myoglobin are observed. The CPK level, which has been linked to the development of kidney failure and mortality, is the most sensitive indicator of crush syndrome. The first line of defense against hyperkalemia, skeletal muscle, is rapidly disrupted during rhabdomyolysis. The result is a particularly risky fulminant hyperkalemia because cardiotoxicity is enhanced by hypocalcemia and shock. Muscle disruption may be associated with immediate critical hyperkalemia (7 to 9.5 mEq/L). In these cases, cardiac arrest can occur in the hour following removal of the limb.

La conjunción de orina oscura, elevación importante del nivel plasmático de creatinfosfocinasa e insuficiencia renal en un paciente con antecedentes traumáticos establece el diagnóstico.[9]​ Sin embargo, en los pacientes traumatizados existen otras causas de insuficiencia renal, entre ellas la hipovolemia, la sepsis y los fármacos nefrotóxicos que se emplean para tratarlos. En un caso de rabdomiólisis el análisis de orina mostrará positividad para microhematuria en las tiras reactivas habituales (por la presencia de pigmento hemo) con ausencia de eritrocitos en el análisis microscópico de la orina. La concentración sérica de creatinfosfocinasa, que aumenta siempre en los pacientes con rabdomiólisis, llega a valores mil veces más elevados que los normales. El nivel máximo de esa enzima se alcanza alrededor de veinticuatro horas después del daño muscular, con un rápido descenso posterior.[9]​ Existe poca correlación entre los valores máximos de creatinfosfocinasa y los niveles de creatinina. Es raro que se desarrolle una insuficiencia renal aguda cuando el nivel de creatinfosfocinasa no supera las 10 000 unidades internacionales (U/L).

En el terremoto ocurrido en Japón en 1995 (gran terremoto de Hanshin-Awaji) el ochenta y cuatro por ciento de las víctimas con valores de creatinfosfocinasa superiores a 75 000 U/L requirieron diálisis en comparación con el treinta y nueve por ciento de los pacientes que no superaron esa cifra. La liberación del potasio intracelular puede generar una hiperpotasemia grave y hasta desproporcionada con respecto al grado de insuficiencia renal, con elevaciones sostenidas y rápidas a pesar de la ausencia de aportes exógenos.[9]​ Las alteraciones del calcio sérico son frecuentes en el síndrome de aplastamiento.

Al principio suele haber hipocalcemia debida al aumento de los niveles de fósforo y al depósito de fosfato de calcio en el músculo lesionado pero durante la fase de recuperación es más común la hipercalcemia por movilización del calcio que se había depositado en el músculo y la corrección de la hiperfosfatemia que genera una mejoría de la función renal. La detección de niveles elevados de aspartato transaminasa (AST), alanina transaminasa (ALT) y lactato deshidrogenasa (LDH) es frecuente y puede ser el primer hallazgo de laboratorio. En este contexto la elevación del nivel de esas enzimas no debe interpretarse como signo de lesión hepática si no se acompaña de otros datos compatibles con ese diagnóstico.[9]​.

in the field

The presence of myoglobin is suggested by the reddish or dark color of the urine (hematuric urine) and ortholidene test strips (urinalysis strips) are used to detect it locally. The solubility of myoglobin in urine is given by urinary pH and therefore the modification of this variable with medications is one of the treatment modalities. A urinary pH less than 5 (acidic) precipitates more than seventy percent of myoglobin, which quickly leads to kidney failure. A urinary pH greater than 6.5 precipitates less than five percent of myoglobin. A pH above 7.5 prevents precipitation and protects the kidney from imminent failure.

Differential diagnosis can be established with a spinal cord injury due to intact sphincters in cases of entrapment of both lower extremities.[7]​.

Según Michaelson, el objetivo principal del tratamiento de los pacientes con lesiones por aplastamiento debe ser evitar que desarrollen el síndrome homónimo, que se asocia con una tasa elevada de morbilidad y mortalidad.[25]​ Siempre según ese autor, el tratamiento de las extremidades afectadas es objeto de controversias. Todavía hay muchos médicos que creen que la similitud que existe entre los signos de las lesiones por aplastamiento y el síndrome compartimental exige que se los trate de la misma manera,[29]​

es decir con una fasciotomía temprana.[25]​ Sin embargo, ese procedimiento no da buenos resultados y es la causa de las pocas muertes informadas en la bibliografía.[25]​.

El síndrome de aplastamiento es una secuencia predecible de complicaciones que siguen a una lesión por aplastamiento. Las lesiones importantes de los tejidos blandos predisponen a los pacientes a múltiples complicaciones entre las que figuran cambios fisiológicos que incluyen hipovolemia, síndrome compartimental, rabdomiólisis, desequilibrios electrolíticos y ácido-base, coagulopatía e insuficiencia renal. Es fundamental tomar las medidas necesarias para reducir al mínimo las complicaciones mediante una evaluación precisa y la implementación de intervenciones terapéuticas correctas.[30]​.

Amputation

The most drastic response to crushing under fallen structures or other objects may be field amputation. In the description of one of his four cases (case I) Bywaters[3]​ commented that prevention through early amputation had been considered adequate but it was later found that it was evident that thirty-six hours was not early enough. His conclusion was that if there was an alternative that would allow immediate amputation to be avoided, it would only be found with a deeper and more complete investigation of these patients, through careful observation of the effects of the treatment or if the condition could be reproduced in the laboratory and, according to him, studies were already being developed at his institution to induce this state under experimental conditions.[3]​ According to the Emergency Medical Services Agency of the city of San Francisco "San Francisco (California)"),[31]​ if the entrapment is endangering the life of rescuers or the patient, field amputation should be considered. The protocol of that institution indicates that in these cases the incident commander be consulted about possible environmental threats to the rescue and contact be established with the doctor at the base hospital to set up a surgical team at the scene of the amputation.[31]​.

The lingering effects of crush syndrome can be fatal even days or weeks after rescue. According to the author of one publication,[24] in a study of eighteen patients admitted to an intensive care unit after the 1999 earthquake in Marmara (Turkey), it was found that eight of them had not survived their stay in the hospital. In the earthquake that occurred on January 12, 2010 in Haiti, doctors faced a particularly difficult situation because although crush syndrome can be managed by strictly monitoring electrolyte levels, in Haiti medical centers had been destroyed by the earthquake, modern equipment was scarce, and electricity was difficult to obtain. Therefore amputation, whether in the field or in an operating room, was often the safest option.[24]​.

The author of this work on the earthquake that affected the population of Haiti in January 2010 wonders if it is possible to die from the crushing of a limb and, obviously, his answer is affirmative.[24] If compression of an arm or leg occurs for less than four hours (a period that is reduced to two hours if it is an elderly person or a person with circulatory problems) there is a good chance that the doctor will be able to save the life and limb of the person. affected person.[24]​ On the other hand, if a person with a limb compressed for more than eight hours survives (because they do not have an open fracture or have succumbed to blood loss) they will most likely require amputation but will otherwise do well. Between these two periods, the decision that doctors must make is difficult because they may try to save a victim's arm or leg but the toxins released by the damaged tissues could enter the circulation, which would imply a high risk of multiple organ failure.[24]​.

During the first phase of crush syndrome the limb is still trapped under concrete or other material structures and therefore without blood flow in any direction. As a result, muscle tissue begins to die and collapsed cells release proteins, potassium, and lactic acid.[24] Those chemicals, which under normal circumstances circulate through the body in much lower concentrations, accumulate in the affected area. Dead muscles also tend to stiffen and if the compressed limb shows a wood-like consistency similar to rigor mortis, it will most likely need to be amputated.[24]​.

Finally, according to specialists in this syndrome, although it is feasible to completely extract a patient in stages, adequate physiological preparation is mandatory: in crush syndrome the conventional procedures for prehospital care are fluid replacement and permissive hypotension.[32][33]​.

Permissive hypotension

The term permissive hypotension refers to the therapeutic procedure implemented in patients with active hemorrhage before surgical control without modifying the systolic blood pressure (SBP) (which is maintained between 80 and 90 mm Hg) with the purpose of sustaining tissue perfusion without exacerbating hemorrhage. The scientific bases of this therapeutic modality are found in experimental studies in which it was demonstrated that attempts to achieve normal values ​​of systemic blood pressure before achieving control of hemorrhage are associated with the risk of increased blood loss and mortality.[32][33]​.

According to another publication, hypotensive resuscitation (or permissive hypotension) in the context of traumatic injuries can be defined as the deliberate decision to allow blood pressure to remain below normal until any active bleeding has been controlled.[34]​.

The dangers of aggressive fluid resuscitation of trauma patients were recognized as early as World War I, but until recently this type of resuscitation was the mainstay of trauma management. Aggressive resuscitation of the polytraumatized patient is based on animal studies in the 1950s and 1960s, studies that used models of controlled hemorrhage instead of uncontrolled hemorrhage.[34] Consequently, any hypotensive polytraumatized patient was synonymous with aggressive fluid resuscitation until reaching normotension before reaching surgery, which determined that preoperative mortality from trauma did not improve and that it was anemia. acute caused by bleeding the reason for the fatal outcome.[35]​ The physiological response of the body consists of stopping the hemorrhage and trying to maintain blood flow to the vital organs while aggressive resuscitation increases bleeding because it prevents this response and ruptures the immature clot formed, which increases mortality.[35]​ Most of the studies carried out in animals and the few carried out in humans have shown that hypotensive resuscitation, which consists of infusing fluids only until If the patient has central pulses (systolic blood pressure between 60 and 70 mm Hg), it allows more patients to reach the operating room alive so that bleeding is controlled and wounds are corrected, a fundamental objective of the traumatized patient who is hypotensive.[35]​.

Mortality and the risk of renal failure are higher in patients with CPK values ​​greater than 75,000 U/L.[36]​ According to the same publication,[36]​ the number of compressed limbs allows immediate estimation of the severity of the syndrome. The authors of the publication just mentioned[36]​ demonstrated that crushing of a limb is related to CPK levels of around 50,000 U/L, a value that reflects the extent of underlying muscle damage.

Crushing of one, two, or three limbs is associated with a fifty, seventy-five, and one hundred percent incidence of kidney failure, respectively. On the other hand, it has been found that the combination of an age greater than fifty-five years, an ISS (Injury Severity Score) greater than sixteen, and a CPK value greater than five thousand is associated with a probability of kidney failure of forty-one percent, compared to a probability of three percent if none of these three risk factors exist.[26]​.

The causes of death of patients with crush syndrome without adequate treatment can be divided into immediate and late. Immediate causes include severe head trauma, traumatic asphyxia, early thoracic injuries, hyperkalemia, and hypovolemic shock. The late ones are kidney failure, coagulopathy, hemorrhage and sepsis.[26]​.

The morbidity and mortality rates of crush injuries are high but there is little data on the functional evolution of the extremities affected by this type of injury.[26] Experience in the functional recovery of the extremities is good, particularly in patients who do not undergo a fasciotomy, and despite the wide variety of injuries to which the kidneys of people with crush syndrome are exposed, chronic renal failure has not been described as a complication of acute renal failure in rhabdomyolysis. traumatic.[26]​.

Crush syndrome, as already mentioned, is the systemic manifestation of rhabdomyolysis caused by continuous and prolonged compression of muscle tissue, that is, a reperfusion injury resulting from traumatic rhabdomyolysis. According to one publication,[37] this syndrome can be prevented and treated if medical personnel take into account that patients with crush injuries often present few signs and symptoms and therefore maintain a high index of suspicion during treatment. According to the same author[37]​ the obstacles that must be avoided to respond correctly to a disaster, for example the collapse of a building, are the lack of planning of evacuation routes before the event occurs, the lack of knowledge about who commands the rescue operations in the disaster area, the delay in the treatment of victims after their extraction from the rubble, the delay in the administration of intravenous fluids, a low index of suspicion in cases of injury due to crushing and discontinuation of monitoring of patients at high risk of acute renal failure, among others.[37] A slow and progressive restoration of blood circulation to the compressed region once it is released is recommended, particularly if the crush lasted for several hours. To prevent toxic substances released by the damaged muscle from suddenly entering the general circulation, a compressive bandage on the affected limb or region and a proximal tourniquet, which will be loosened frequently, are recommended. The compressive bandages and tourniquet will be applied immediately after decompression, without allowing any delay.[37]​.

Despite the publication of a detailed description of the clinical picture of four cases of crushing by Bywaters and Beall in 1941,[3] disaster-related crush syndrome went unnoticed until one of the deadliest earthquakes of all time, the Tangshan earthquake of 1976.[5] That earthquake killed 240,000 people and injured 165,000 and In the context of that catastrophe, three important observations were made, namely, the incidence of crush syndrome varied from two to five percent among injured victims, patients with crush injuries, whose general condition appears satisfactory, can die suddenly due to hyperkalemia and finally, regardless of the severity of muscle compression, any patient can develop crush syndrome; Therefore, all cases of crushing should be closely observed for any incipient signs of acute renal failure.[38]​ Those observations were confirmed by several subsequent earthquakes.[39]​[40][41]​.

In 1979 and 1982, respectively, two interesting events were observed that had a great impact on the subsequent therapeutic attitude towards disaster-related crush syndrome. In 1979, seven victims trapped after the total collapse of a building were extracted from the rubble after twelve hours and received the first post-rescue intravenous infusion with a delay of six hours. All of these patients developed acute renal failure within the first day after rescue despite having received volume replacement of between five and ten liters of saline per day.[42] By contrast, in 1982, in a similar incident, of eight patients who were trapped under the rubble of a building, seven began receiving intravenous fluids immediately—even before complete removal—at the site of the collapse. Within two hours of their release, these patients were transferred to a hospital where forced volume replacement treatment with alkaline solutions was continued. None of them developed acute renal failure. The remaining patient, who had been buried under rubble for five and a half hours, once freed was transported to a trauma center after a twenty-four hour delay and until then had only received two liters of intravenous fluid. Upon arrival at the center, this patient had already developed established acute renal failure, the treatment of which required supportive dialysis for a month.[43] These observations underscore the vital importance of crush victims receiving fluid replacement as soon as possible, if possible before extraction.[5]

The concepts "renal disaster", "seismonephrology" and "disaster nephrology" have evolved.[5] During the 1988 Armenian earthquake, which caused around 150,000 deaths, rescue teams arrived at the disaster zone with considerable delay and found that about six hundred victims who had been rescued from the rubble after the fact had developed acute kidney failure, after which many of them had died from lack of dialysis.[44]​ In fact, that event was the origin of the term "renal disaster." The extensive support that Armenia received from abroad was of little use[45]​ because at that time there was no organized international support structure available.[46]​ Later the International Society of Nephrology founded the organization called Renal Disaster Relief Task Force (RDRTF),[note 2]​ a global body of kidney experts whose volunteers (doctors and nurses) provided their help for the first time in the 1999 İzmit Earthquake in Turkey, where four hundred and sixty-two people received dialysis with positive results.

Of the six hundred and thirty-nine patients with crush syndrome recorded in the 1999 Marmara earthquake, four hundred and seventy-seven required dialysis support and more than five thousand dialysis treatments were applied.[49] Among all subsequent well-documented earthquakes the largest number of patients with acute renal failure related to crush injuries was reported after the Kobe disaster in Japan in 1995, with two hundred and two cases.[36]

According to an already mentioned publication,[43]​ to prevent systemic complications in patients with crush injuries, aggressive fluid treatment should be administered. Furthermore, the authors of the work clarify that to achieve this purpose it is not necessary to excise dead muscle.[43] On the other hand, according to them, an open crush injury requires fasciotomy and immediate radical debridement of the dead muscle tissue and may also require amputation through healthy tissue in an extremity with significant skin laceration. Finally, the same publication advises that a closed crush injury should not be treated surgically until there is demarcation of a gangrenous portion. Even obvious extensive myonecrosis is not an indication for immediate surgical treatment. The only exception to this precept is the need to perform a fasciotomy to save the distal part of the limb if there are no distal pulses or capillary refill and the fasciotomy must be accompanied by radical debridement.[43]​.

Another author[50]​ maintains that the hospital management of crush injuries is essentially that of rabomiolysis. Surgical management is similar to that adopted in all trauma cases. According to him, very aggressive fluid resuscitation, diuresis with fasciotomies when indicated, and monitoring of enzymes and electrolytes will save many limbs and many lives.[50]​.

According to a 2004 publication already mentioned,[41]​ the first objective that should be pursued in the care of disaster victims is to prevent the development of crush syndrome, which can best be achieved through early and massive fluid administration.[41]​ Acute kidney failure resulting from rhabdomyolysis is a major cause of morbidity and mortality in victims rescued from disasters, so its prevention is vital to reduce the number of deaths.[41]​ Since Hypovolemia is the most important factor in the pathogenesis, early and vigorous fluid resuscitation is the most useful therapeutic measure in the prophylaxis of this disorder.[51]​[52]​ The effectiveness of this approach was first demonstrated in victims of crush injuries during a building collapse[42]​ and was subsequently confirmed in victims of the Kobe earthquake, Japan,[41]​ and in a pediatric subgroup of the Marmara earthquake, Turkey.[53]​ However, extensive and uncontrolled fluid resuscitation can cause hypervolemia and related complications, especially in elderly patients and in those in whom treatment is significantly delayed.[51]​ Therefore, fluid resuscitation must be individualized taking into account various medical and logistical variables, namely demographic characteristics, scale of the disaster, environmental conditions, time spent under debris, length of the extraction procedure, volume status and diuresis.[51]​ Because crush syndrome can be avoided with aggressive fluid management,[41]​ patients with crush injury should never be left without treatment, even when dialysis is not available.[54][55]​.

Finally, the best preventive measure to reduce the number of victims of a disaster is to build high-quality buildings. In some cases fixing furniture to walls can also be useful. In the absence of such measures the incidence of disaster-related crush injuries will remain high.[40]​[56]​.