Severe crush injury in adults

INTRODUCTION — Severe crush injury results from direct physical trauma to the torso, extremities, or other parts of the body from an external crushing force. Severe compression results in direct tissue trauma and sequelae of ischemia-reperfusion injury. Once the compressive forces are released, muscle injury and swelling can occur, with possible muscle necrosis and neurologic dysfunction in the affected areas. Systemic manifestations resulting from crush injury, which is defined as crush syndrome, can result in organ dysfunction or death. It is imperative that rescuers and health care professionals recognize crush injury to avoid missing a narrow window of time in which to provide intensive fluid resuscitation, which may limit acute kidney injury.

Severe crush injury in adults is reviewed. Prevention of crush syndrome and other causes of rhabdomyolysis are reviewed separately. (See "Pathophysiology, classification, and causes of acute extremity compartment syndrome" and "Crush-related acute kidney injury" and "Rhabdomyolysis: Epidemiology and etiology".)

DEFINITIONS AND MECHANISM OF INJURY

Crush injury — Crush injury is the result of physical trauma from prolonged compression of the torso, limb(s), or other parts of the body. The resultant injury to the soft tissues, muscles, and nerves can be due to the primary direct effect of the trauma or ischemia related to compression. In addition to possible direct muscle or organ injury, after the release of the compressive force, severe crush injury results in swelling in the affected areas, with possible muscle necrosis and neurologic dysfunction. This soft tissue injury can also be due to a secondary injury from subsequent compartment syndrome.

Nontraumatic presentations of crush injury include patients with prolonged immobilization while intoxicated or under anesthesia. In such cases, the weight of the body part alone without relief may produce compartment syndrome and rhabdomyolysis. Other causes of impaired consciousness such as stroke or coma can also result in prolonged immobilization with crush injury. The affected muscle compartment may be the one lying on a hard surface or may be caused by one extremity crossing over another, increasing local pressure. Gluteal compartment syndrome has been described in postoperative, intoxicated, and comatose patients with prolonged immobilization and may lead to crush syndrome, especially as presentation or recognition is frequently delayed [1]. Other causes of nontraumatic crush syndrome have been described, including ischemic, metabolic, toxicologic, and oncologic causes of rhabdomyolysis.

●(See "Rhabdomyolysis: Epidemiology and etiology".)

●(See "Rhabdomyolysis: Clinical manifestations and diagnosis".)

Crush syndrome — Crush syndrome is defined as the systemic manifestations resulting from crush injury, which can result in organ dysfunction (predominantly acute kidney injury [AKI], but multisystem organ injury can also occur), or death [2-5]. The manifestations of crush syndrome are the systemic consequences of muscle injury, specifically rhabdomyolysis, which commonly result in AKI.

Crush syndrome can also manifest in other situations where there is compression of the tissues. As examples, the crushing of tissues can occur with prolonged immobilization, or from burns or electrical injury where tissues are compressed by unyielding fascia or burned skin causing a compartment syndrome. Crush syndrome is the second leading cause of death in earthquakes, following direct trauma.

Mechanism of injury — Typical causes of crush injury include being trapped under a vehicle or related to industrial, construction, or agricultural accidents [6,7]. In natural disasters such as major earthquakes, 3 to 20 percent of mass casualties may involve crush injuries due to building collapse and entrapment [8,9]. Mass crowd stampedes can cause crush injuries as well as traumatic asphyxia [10]. (See 'Traumatic asphyxia' below.)

The compressive force causes direct tissue damage while occluding venous outflow. With prolonged compression, the resultant cellular death, in particular myonecrosis, may lead to crush syndrome. Clinical deterioration including death can occur within 20 minutes of extrication, leading to the nickname of "smiling death". The victim, smiling after extrication and rescue, suddenly arrests from ventricular fibrillation from the efflux of potassium, phosphorus, and myoglobin from the areas of injury. Delayed complications and death that occur as a result of renal failure were well documented in patients extricated from collapsed buildings during historic earthquakes and during the 1941 London Blitz bombings [4,5].

Primary prevention of crush injury might be possible only via industrial safety regulations, building codes, and injury prevention programs. Once a crush injury has occurred, secondary prevention of crush syndrome may be possible with timely management at the scene of injury and carried on through field care, prehospital transport, and initial hospital care. (See 'Extrication and on scene management' below.)

EXTRICATION AND ON SCENE MANAGEMENT — Patients with crush injuries are often trapped at the scene. Individual victims or small numbers of individuals experiencing injury may be extricated by bystanders or professional rescuers and receive prehospital care via emergency medical services (EMS).

However, large-scale mass trauma events such as earthquakes and major building collapses in natural or manmade disasters may entrap dozens to thousands of victims. This may require the deployment of Urban Search and Rescue teams (USAR), which in the United States are in partnership with local fire departments, law enforcement agencies, federal and local governmental agencies, and private companies.

Extrication time is strongly associated with earthquake-related mortality. Children and older individuals are highly vulnerable. Entrapment >24 hours is highly associated with mortality. A limited number of survivors may be extricated from 48 hours to 14 days later [11]. Survivors are frequently found in voids in the collapsed structure. Most deaths occur in victims trapped beneath rubble who received forces too great to withstand; other causes of death include dust inhalation, traumatic asphyxia, head injury, or multiple injuries. In addition, in many events, rescuers may comprise a significant percentage or even a majority of casualties. Extrication of victims from collapsed structures is hazardous, and the risk of secondary collapse is significant.

Confined space medicine — Since extrication of victims may require tunneling and supporting debris, and victims may be physically entrapped, "scoop and run" is often not possible, requiring initial crush injury care and crush syndrome prevention to be provided by rescuers inside the structure termed "confined space medicine" (CSM) [12]. Delivery of medical care in such environments is hazardous and requires special training with attention to managing hazards such as dust, temperature extremes, hazardous materials and gases, fire, explosions, secondary collapse, and providing care while wearing personal protective equipment. The safety of the rescuers is paramount, and safety is the responsibility of the scene incident commander and the incident command system [13].

While most mass crush injury events are associated with earthquakes, terrorist bombings are increasingly a cause of structural collapse. In these circumstances, crush injuries may be associated with blast injury, fire, or toxic inhalation. Local endemic diseases may also represent a threat to victims and rescuers.

Support of airway, breathing, circulation — Crush injury to the chest is a significant source of respiratory failure and death. Patients may require oxygen, airway adjuncts such as oral and nasal airways, intubation (at times a surgical airway), and the use of portable ventilators. Inhalation injury due to dust or associated with hot gases, such as in fire or bombings, can also require advanced airway management. Provision of CSM trauma care may require airway management in unusual positions and orientations. (See "Inhalation injury from heat, smoke, or chemical irritants".)

Pneumothorax, hemothorax, flail chest, and pulmonary contusion may require chest decompression (eg, needle or finger decompression, chest tube) during extrication care. (See "Initial evaluation and management of chest wall trauma in adults" and "Thoracostomy tubes and catheters: Indications and tube selection in adults and children".)

Hypovolemia may be due to a number of reasons. For patients with prolonged entrapment, dehydration is a common cause of hypovolemia and is a leading cause of death. Hemorrhage, third spacing, and burns may also cause hypovolemia. Hemorrhage from traumatic injuries may be delayed due to compression of wounds or organ injuries until after extrication. Immediate management of hypovolemia and prevention of crush syndrome and death from post-release hyperkalemia requires rapid access with large-bore intravenous catheters and administration of isotonic saline. Potassium-containing solutions should be avoided. Crush injury without adequate fluid resuscitation develops into crush syndrome. Urine output is monitored during prolonged field care. (See "Crush-related acute kidney injury".)

USAR teams, CSM paramedics, and EMS paramedics use fluid administration algorithms to prevent crush-related acute kidney injury [13]. Typically, a 1000 mL/hour bolus of normal saline is initially administered to adults for two hours, then reduced to 500 mL/hour (algorithm 1) [14,15]. Smaller volumes such as 10 cc/kg are recommended for those with known heart failure, renal failure, or chronic obstructive pulmonary disease.

Extremity reperfusion and hyperkalemia — Upon release of a trapped extremity, patients can have minimal symptoms and the extremity may be only mildly erythematous or ecchymotic, or it can be obviously mottled and ischemic.

Any pain can be managed with opioids or ketamine according to local EMS protocols [16].

The release of potassium from injured and necrotic muscles and other tissues can lead to a rapid onset of hyperkalemia and ventricular fibrillation. Prehospital administration of intravenous crystalloid is the mainstay of treatment (algorithm 1) and is associated with improved outcomes. (See "Crush-related acute kidney injury", section on 'Prevention of hyperkalemia' and "Treatment and prevention of hyperkalemia in adults".)

A prehospital electrocardiogram tracing can detect the peaked T-waves and widened QRS of hyperkalemia and can be treated by the paramedic (table 1). This is appropriate depending on local medical direction.

Tourniquets should otherwise only be used to control extremity bleeding. Do not use tourniquets to isolate a crushed limb in the field. Placement of tourniquets with intent of preventing the release of potassium and other cellular contents into the circulation from a crushed extremity has not been supported by evidence and is not recommended [14,15]. An exception may exist in resource-limited environments when fluid resuscitation and monitoring are not immediately available. The United States Department of Defense Joint Trauma System (JTS) Clinical Practice Guideline (CPG) states that a tourniquet may be placed on the affected extremity prior to extrication to help prevent crush syndrome when the time of entrapment is anticipated to be greater than two hours [17]. (See 'Extremity crush injury' below.)

Similarly, prophylactic fasciotomy should not be performed in the field due to the risk of infection [15]. (See 'Mangled extremities' below.)

Furthermore, prehospital amputation of severely crushed or mangled limbs solely to avoid crush syndrome is also not supported by evidence and increases the risk of stump infection. However, amputation may be needed as a last resort to extricate a victim. (See 'Field amputation' below.)

Field amputation — Some patients who are trapped have extremities that cannot be extricated from debris or structure in a timely fashion (eg, structural failure imminent). In such cases, amputation in the field may be required as a last resort for extrication. Manual or powered saws have been used depending on available space, resources, and risk of explosive gases. (See "Techniques for lower extremity amputation".)

In some jurisdictions, the protocol may include an incident-command trained surgical emergency team from a trauma center to provide surgical expertise beyond the paramedic's scope of practice. Whenever possible, a surgical team, if available, should be dispatched to perform this procedure. Typically, a tourniquet is applied and a guillotine amputation as distally as possible is performed, although a through-knee amputation may be appropriate if the lower leg is nonviable. Anesthesia and analgesia should also be provided as tolerated. Suggestions for appropriate drugs and equipment safe for use in confined and hazardous environments are available and reviewed in the reference [18].

Triage and transport — Triage at the scene, rapid transport of "immediate" triage category patients via cleared routes, and retriage at the hospital are essential for optimal survival (algorithm 2).

Scene triage usually uses three categories to determine priority to receive treatment at the scene and transport: "immediate" patients are treated and transported first, followed by the "delayed" category. "Minor" category patients may be treated and released at the scene or transported last. An "expectant" category is often used for patients with a low likelihood of survival, such as postcardiac arrest patients, severe head injuries, patients in persistent shock, and patients with massive burns; these patients may receive palliative care (figure 1). In many events, some patients who were classified as "expectant" ultimately survived, so retriage of all cases is necessary. (See "Overview of the management of the severely burned patient", section on 'Mass casualty events'.)

The majority of patients, typically 80 to 85 percent in mass casualty events such as earthquakes, require only basic medical care without major procedures or organ support. Typically, in bombings with building collapse scenarios, approximately 50 percent of patients arrive at the facility in the first hour and have lower acuity and higher survival than the remaining half, who will arrive over the next eight hours or more [8,19,20]. Lower acuity patients should be triaged quickly, treated rapidly, and discharged. Many facilities will use alternative external spaces to triage directly outside the facility to prevent patients with minor injuries from even entering the hospital [14]. This avoids filling the hospital before more severely injured patients arrive. Only approximately 15 to 20 percent of earthquake casualties will require hospitalization, major procedures, or organ support. This latter group is at risk of death, and mortality in this group is termed the "critical mortality rate."

Secondary transport may be limited by the condition of the patient; some crush injury patients may have hemorrhage from wounds or internal injuries, hemorrhagic shock, hyperkalemia, and respiratory failure, which may reduce the distance the patient is able to travel or may require critical care transport logistics. In situations of overwhelmed and destroyed local resources, triage decisions may be needed to determine those likely to survive transport and subsequent care. Patients with a low likelihood of survival, such as post-cardiac arrest patients, severe head injuries, patients in shock, patients with massive burns, or patients with multiple organ failures, may not be good candidates for secondary transport. (See "Overview of the management of the severely burned patient", section on 'Triage and transfer' and "Overview of the management of the severely burned patient", section on 'Combined burn/trauma'.)

CLINICAL MANIFESTATIONS — Crush injury refers to trauma caused by a direct crushing force. In addition to the direct tissue damage, the compressive force prevents venous outflow, leading to accumulation of potassium, phosphorus, and myoglobin in the tissues. Venous obstruction may be also associated with extremity edema.

Traumatic asphyxia — Severe crush injury to the chest (eg, heavy object, stampede) can result in traumatic asphyxia. This is due to the significant increase in the thoracic pressure and pressure within the superior vena cava; this increased pressure in addition to attempts at inspiration against a closed glottis can lead to capillary rupture in the head and neck. The classic appearance is [21,22]:

●cervicofacial cyanosis

●edema

●subconjunctival hemorrhage

●petechial eruptions on the face, neck, and torso above where the object was compressing the victim

●This injury is typically seen after a short duration of crushing forces (only a few minutes), as more than a few minutes of asphyxia results in death. Traumatic asphyxia has been seen in crowd crush events, such as stampedes at sports, religious, music, and political events. Victims may also have been trampled and have musculoskeletal injuries and fractures. Traumatic asphyxia may be combined with liver and spleen lacerations, rib fractures, pulmonary contusions, and anoxic brain injury [10].

Hypovolemia — Crush injury patients commonly have hypovolemic shock manifested by tachycardia, prolonged capillary refill, narrow pulse pressure and if severe, hypotension in the first few hours of presentation. This may be from an obvious source due to external hemorrhage from an injured extremity or occult, related to organ injury. Another possible cause of hypovolemic shock in crush injury patients is a distributive shock associated with third spacing and the inflammatory response to the reperfusion injury and cell death [23].

It is critical to recognize and treat the cause of shock to prevent further tissue ischemia and cell death. Hypotension may also worsen the risk of developing subsequent acute kidney injury (AKI). (See 'Sequelae of crush injury' below.)

Extremity crush injury — Crush injury to the extremity can present clinically within a spectrum from generalized swelling and erythema to blisters and purpura to open fractures and mangled extremities with ischemia. In addition to management of the expected orthopedic and vascular issues associated with this type of injury, awareness is needed for the potential of these patients to develop acute compartment syndrome and rhabdomyolysis. These can occur either due to the crushing direct trauma causing tissue swelling or due to the prolonged hypoperfused state causing an ischemia-reperfusion injury that can result in swelling, acute compartment syndrome, and rhabdomyolysis. Prolonged compression can lead to cell death, causing muscle necrosis and rhabdomyolysis [24]. This can be associated with compartment syndrome and systemic manifestations of tissue damage leading to crush syndrome. Prolonged compression of major arteries can also lead to intimal injury and thrombosis, which further exacerbates distal ischemia. (See "Acute compartment syndrome of the extremities" and "Rhabdomyolysis: Clinical manifestations and diagnosis" and "Crush-related acute kidney injury".)

Thoracic or abdominal injury — Blunt injury to the thorax or abdomen can also result in pulmonary contusion, cardiac contusion, rib fractures, pelvic fracture, hemothorax, pneumothorax, and other blunt solid and hollow viscus injuries. Prolonged compression has even been associated with spinal cord injury without fracture [25]. Blunt injury from the crush mechanisms can be complicated by concomitant penetrating injury as a result of projectiles. (See 'Organ injury' below.)

Sequelae of crush injury

Acute kidney injury — (AKI) — The development of AKI can be multifactorial. While crush syndrome can cause AKI due to the directly nephrotoxic effects of heme products and the tubular obstruction by myoglobin and urate crystals, hypotension and hypoperfusion can also contribute to acute tubular necrosis [23]. Crush-related AKI manifests as rhabdomyolysis and myoglobulinemia, hyperkalemia, hyperphosphatemia, and myoglobinuria. (See "Crush-related acute kidney injury".)

The prognosis for those with AKI who survive and do not become chronically dialysis-dependent is good. Older individuals and those with chronic kidney disease are at increased risk for progression to end-stage kidney disease. Even with optimal circumstances, the risk of dialysis is approximately 10 percent [26].

Acute respiratory distress syndrome — Acute respiratory distress syndrome can also occur following severe crush injury. Contributing factors can be large-volume crystalloid resuscitation, the inflammatory response to injury, tissue necrosis, distributive shock, or fat embolism syndrome associated with long-bone fractures. (See "Crush-related acute kidney injury" and "Fat embolism syndrome" and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults".)

HOSPITAL MANAGEMENT OF SEVERE CRUSH INJURY

Initial trauma management — The initial management of trauma patients at the emergency department is described in the Advanced Trauma Life Support program. (See "Initial management of trauma in adults".)

Administration of isotonic saline initiated in the field should be continued with close monitoring of urine output (algorithm 1).

Ongoing trauma management — The management of patients with crush injury includes all the components of care used for other trauma patients. (See "Overview of inpatient management of the adult trauma patient".)

Clinical monitoring — Clinical examination and laboratory studies should be performed several times each day until stabilized. These include electrolytes (particularly serum sodium, potassium, and bicarbonate), creatinine, and arterial blood gases with lactate and/or base deficit. A urinary bladder catheter should be placed upon admission for close monitoring of urine output.

For patients with an overt history or history suggestive of crush injury, the patient should be monitored continuously, and electrolytes (particularly potassium, calcium, and phosphate) and arterial blood gas should be obtained. Urine myoglobin and creatine kinase can be obtained to detect rhabdomyolysis. (See "Rhabdomyolysis: Clinical manifestations and diagnosis" and "Clinical features and diagnosis of heme pigment-induced acute kidney injury" and "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)

Mangled extremities — Some extremity crush injuries are so severe, the injured limb will be of questionable viability. The need for amputations varies widely (3 to 59 percent) depending on delays in extrication, associated injuries, and local resources. Guidelines suggest that amputation should be restricted to cases where a limb is nonsalvageable or when injuries to the limb are causing sepsis, systemic inflammation, or uncontrollable hemorrhage [14]. Decision-making regarding limb salvage is clinical; scoring systems such as the mangled extremity severity score (MESS) have not been shown to be predictive and have worse performance compared with the judgment of experienced surgeons. In a mass casualty situation, the resources such as blood transfusion needed to attempt limb salvage may be inadequate, and amputation may be more likely to be necessary. (See "Severe upper extremity injury in the adult patient" and "Severe lower extremity injury in the adult patient" and "Surgical management of severe upper extremity injury" and "Surgical management of severe lower extremity injury".)

Severe crush injury is a known cause of acute extremity compartment syndrome. Early recognition, evaluation, and treatment of compartment syndrome reduces the risk of crush syndrome and limb loss. Fasciotomy to fully decompress all involved compartments is the definitive treatment for established extremity compartment syndrome in the great majority of cases [27]. Delays in performing fasciotomy increase morbidity, including the need for amputation. The clinical features of acute extremity compartment syndrome and fasciotomy, including the difference between upper and lower extremities, are reviewed separately. (See "Pathophysiology, classification, and causes of acute extremity compartment syndrome", section on 'Classification' and "Acute compartment syndrome of the extremities" and "Upper extremity fasciotomy techniques" and "Lower extremity fasciotomy techniques".)

Prophylactic fasciotomy for severe crush injury is not recommended even in the situation of mass crush injury events, and we do not perform prophylactic fasciotomy in this clinical situation. We typically perform fasciotomies only if established acute compartment syndrome is present clinically on admission or if measured compartment pressures demonstrate a difference between the diastolic blood pressure and the compartment pressure (delta pressure) of 30 mmHg or less. Impending compartment syndrome in indeterminate cases might be suspected by rising measured compartment pressures and is managed by serial examinations, and may lead to fasciotomies as the delta pressure falls to 30 mmHg or less. In several earthquake studies, routine use of fasciotomy in crushed limbs has not led to improvement in outcomes, but rather to higher rates of bleeding, infection, and amputation [28-31]. In resource-limited environments, good outcomes from fasciotomy seem less assured, and a more limited role for fasciotomy may be appropriate to avoid unnecessary fasciotomies and excess infections. Such fasciotomies consume scarce operating room time and increase wound-care workload when resources are limited. In such scenarios, some authors recommend that fasciotomy in severely crushed limbs be performed only in established acute compartment syndromes, when distal pulses are significantly diminished or lost [14,28,32].

Fasciotomy for late compartment syndrome, after eight hours, is generally not recommended. Extensive myonecrosis is very likely to be present, and performing fasciotomy obliges the clinician to perform serial surgical debridements and to monitor the wound and patient carefully for wound sepsis and systemic problems, such as rhabdomyolysis and renal failure. The authors recommend avoidance of late fasciotomy in resource-limited events.

Organ injury — Torso crush injuries are associated with solid injuries, including hepatic and splenic lacerations, as well as hollow viscus injuries. The likelihood of these injuries may be increased in structural collapses caused by bombings. Mortality rates are higher for those with associated thoracic or abdominal injuries. Specific management of traumatic injuries is reviewed separately.

●(See "Management of splenic injury in the adult trauma patient" and "Surgical management of splenic injury in the adult trauma patient".)

●(See "Management of hepatic trauma in adults" and "Surgical techniques for managing hepatic injury".)

●(See "Overview of the diagnosis and initial management of traumatic retroperitoneal injury" and "Management of blunt and penetrating renal trauma".)

●(See "Traumatic gastrointestinal injury in the adult patient".)

●(See "Traumatic and iatrogenic bladder injury".)

Renal replacement therapy and mass casualty events — Once acute kidney injury is established, aggressive intravenous fluid resuscitation is no longer appropriate. Hemodialysis is initiated for the usual indications of volume overload, hyperkalemia, severe acidemia, and uremia. Crush injury can be associated with very rapid and severe onset of hyperkalemia, and hemodialysis may be required two or more times a day to control. (See "Crush-related acute kidney injury", section on 'Treatment of established acute kidney injury'.)

Earthquakes and other mass casualty events leading to large numbers of crush syndrome patients may place severe demands on local health care systems. Mass crush injuries may produce excess demand on dialysis facilities and critical care units, with a need for more dialysis machines and operators as well as ventilators and critical care unit health providers. The need for acute hemodialysis may overwhelm local resources and threaten access for chronic hemodialysis patients. This may require the activation of surge plans, equipment caches, or secondary transport of casualties to areas with still intact infrastructure able to manage these casualties. Critically ill, multiply injured patients in the intensive care unit may require continuous renal replacement therapies, which place additional demands on dialysis resources and personnel. While there are limited data on the optimal technique of continuous renal replacement in rhabdomyolysis, a small trial reported that myoglobin clearance was improved using continuous venovenous hemodialysis with high cutoff dialyzer and regional citrate anticoagulation compared with continuous venovenous hemodiafiltration with regional citrate anticoagulation [33].

Within the United States, the National Disaster Medical System (NDMS) may provide a Crush Injury Specialty Disaster Medical Assistance Team (DMAT), which provides advice to local facilities. Evacuation of dialysis patients to other areas of the United States coordinated by the NDMS is another strategy.

Worldwide, in 1989 the International Society of Nephrology created the Renal Disaster Relief Task Force, which offers personnel, material, advice, and psychological support to support providers and paramedics for any disaster that involves renal disease [34].

When inadequate numbers of hemodialysis machines are available, peritoneal dialysis can be used, despite its slower clearance of potassium [35]. Any mass casualty event can make a severe demand on ventilators and respiratory care providers. All states should have a ventilator allocation plan based on the United States Centers for Disease Control and Prevention influenza planning.

Psychosocial support — Psychologic trauma is a component of crush injury. Family and other caregivers, health care workers, and uninjured victims may also experience shock and grief and later depression and post-traumatic stress disorder. Suicide is a risk for disaster survivors, first responders, and health care providers [36]. Disaster response planning should include plans to provide emotional, psychologic, psychiatric, and social support to all who need it [37]. (See "Posttraumatic stress disorder in adults: Treatment overview".)

MORTALITY — The majority of mortality in mass crush injuries occurs at the scene due to traumatic asphyxia, severe traumatic brain injury, and severe hemorrhagic shock [9]. "Time under the rubble" is an important determinant of survival. Historically, 80 percent of entrapped victims die quickly by the direct effects of trauma or traumatic asphyxia, 10 percent survive with minor trauma, while 10 percent are badly injured. Among those, 40 to 70 percent develop crush syndrome. Other complications of crush injury, including non-acute kidney injury-associated hyperkalemia, acute respiratory distress syndrome, and sepsis, can also lead to death.

Mortality related to crush syndrome varies depending on patient and local factors; patients with rhabdomyolysis-induced renal failure have a mortality of approximately 20 percent, but this rate will be higher in patients with multiple injuries or multiorgan failure and when local resources are overwhelmed [38,39].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General issues of trauma management in adults" and "Society guideline links: Severe blunt or penetrating extremity trauma" and "Society guideline links: Thoracic trauma" and "Disaster management: Links to UpToDate resources and society guidelines" and "Society guideline links: Extremity compartment syndrome" and "Society guideline links: Thoracic and lumbar spine injury in adults" and "Society guideline links: Traumatic abdominal and non-genitourinary retroperitoneal injury".)

SUMMARY AND RECOMMENDATIONS

●Crush injury and crush syndrome – Severe crush injury results from direct physical trauma to the tissues caused by an external crushing force. Crush syndrome can also manifest in other situations where tissue becomes compressed (eg, prolonged immobilization, extremity compartment syndrome). Severe crush injury increases the risk for organ failure and death due to the possible development of crush syndrome, which is the systemic manifestation of crush injury. Severe crush injury to the chest (eg, heavy object, stampede) can result in traumatic asphyxia. (See 'Definitions and mechanism of injury' above.)

●Mass casualty events – Large numbers of severe crush injury patients may occur after natural or manmade disasters with building collapses. Outside of a mass disaster setting, severe crush injury is uncommon. Regardless of cause, survival is directly related to extrication time. Many jurisdictions have urban search and rescue teams for mass disasters that can provide confined space medicine, including management of severe crush injury and prevention of crush syndrome during extrication. Severe demands on resources can occur after a mass crush injury casualty event. Guidelines for hospital management of multiple crush syndrome patients are available, and relief teams for renal disasters can be mobilized. (See 'Extrication and on scene management' above.)

●Clinical manifestations – Clinical manifestations associated with crush injury are many and can involve multiple organ systems. These are reviewed above. Crush syndrome may present with rhabdomyolysis, which manifests with hyperkalemia, hyperphosphatemia, and myoglobinuria. Within minutes of extrication, crush syndrome can produce death due to hyperkalemia and ventricular fibrillation. Acute kidney injury is directly related to the nephrotoxic effects of heme products and tubular obstruction by myoglobin and urate crystals. (See 'Clinical manifestations' above.)

●Prevention of crush syndrome – Crush syndrome can be prevented by the administration of a large-volume intravenous crystalloid administration as soon as possible (algorithm 1), including during extrication of the entrapped patient. (See "Crush-related acute kidney injury", section on 'Prevention'.)

●No role for prophylactic fasciotomy – For patients with crush injury to an extremity, we do not perform prophylactic fasciotomy (ie, fasciotomy before development of impending or established compartment syndrome). Fasciotomy should be performed only for progressing clinical manifestations of acute compartment syndrome associated with confirmed elevation of compartment pressures, particularly in resource-limited settings. (See 'Mangled extremities' above.)