Injuries are typically defined by their mechanism -- those activities or agents that cause the injury. They also are typically characterized by their severity and potential for complications.
Crush injuries are associated with particular mechanisms of injury and can range from mild to fatal in severity. Most importantly, soft tissue injuries resulting from a crush can be a major source of complications, impairment and disability.
Etiology and Mechanism of Injury
Generally, crush injuries are associated with severe trauma and most commonly occur in motor vehicle crashes, industrial or farm incidents, and mass-casualty disasters.
A person may sustain a crush injury as a result of being trapped in a motor vehicle, such as may occur if an extremity is crushed under the weight of a rolled-over vehicle.
Wringer-type farm machinery, rock crushers and large compressor-type industrial equipment can lead to extremity injuries. Construction equipment such as bulldozers and cranes may cause crush injuries to the extremities, chest, abdomen or entire body.
A mass-casualty incident such as a building collapse or bombing also can produce crush injuries. Entrapment under fallen debris can produce significant continuous compression, especially if special equipment is needed or it is unsafe to attempt extrication.
The common denominator in all of these situations is the resultant compression injury to muscles and tissues.
Ischemia and Tissue Damage
The severity of the tissue damage is primarily related to the amount of force applied to the tissue, the length of time that force was applied, and the type of tissue or muscle that was compressed.1
A relatively heavy force applied to any tissue or extremity, even briefly, can produce injury. Although injury may not initially be apparent, patients may develop symptoms of injury once the tissues begin to swell. Prolonged compression of a body part will cause ischemia and anoxia of the tissues. Prolonged ischemia eventually leads to necrosis or death of the tissue and muscles.
Following an injury, such as a crushing blow to an extremity, the tissues will begin to swell. Third spacing of fluids leads to increased edema and more swelling of the body part, further increasing the pressure on the muscles and tissues, causing additional ischemia and anoxia.
The immediate threat to a limb is whether perfusion is sufficient to maintain or continue the viability of the tissues. The more severe the injury or the more prolonged the ischemia, the less viable the tissues and extremity become.
Should other injuries be present that produce life-threatening problems for the patient, such as shock, the ischemic and anoxic potential for the affected extremity is significantly increased and may lead to an irreversible condition.
Types of Compression Injuries
Tissue compression injuries can produce crush wounds, degloving-type wounds or traumatic amputations.
Crush wounds may include abrasions, lacerations, local or systemic hematomas and contusions. Although the injury initially may seem minor or not life-threatening, blood vessels, nerves and other internal structures lie under and within the soft tissues and can produce a far greater problem to the patient over time.
Degloving injuries occur from shearing-type forces and can cause severe soft tissue destruction. These injuries can range from a skin avulsion or a flap-type wound to a full-thickness injury or a total loss of tissue and bone. This can result in not only significant skin integrity disruption but also loss of the function of the extremity.1
Traumatic amputations can involve both the upper or lower extremities. A complete amputation occurs when there is complete detachment of the part from the body. Incomplete amputations still have some connecting tissue attached.1
Immediate Action Essential
Three major syndromes are associated with crush injuries and can result in severe metabolic abnormalities and significant complications for the patient.
Compartment syndrome is a result of increased pressures within a closed muscle compartment. This syndrome accounts for approximately 2 percent of all malpractice claims in the United States, the claims primarily related to the condition being unrecognized or untreated.2
If the diagnosis is made, an immediate consultation with an orthopedic surgeon is warranted. This syndrome is time dependent and limb threatening. If untreated, the associated edema and ischemia can result in muscle death or permanent loss of function of the extremity.
The diagnosis of compartment syndrome is made on clinical findings, the history of the injury, physical signs and symptoms, and a high index of suspicion.3
The initial symptom often is pain that appears late and is out of proportion to the initial injury. Additionally, because the pressure is increasing in a closed compartment of an extremity, ischemia can quickly ensue if the pressure is great enough to occlude the arterial or venous flow.
However, it is important to remember that capillary refill and distal pulses, those simple-to-check indices of adequate circulatory status, may not change in the early stages of the injury. Pallor, poor capillary refill and pulselessness are not early signs of compartment syndrome.3 They are signs of severe impairment and must be addressed promptly. Parasthesia may be an early complaint but may lead to irreversible damage if ignored or allowed to persist.
Normal compartment pressure is 10 mm Hg or less. If the patient has a compartment pressure exceeding 30 mm Hg and has findings suggestive of compartment syndrome, prompt treatment is essential.2 Management involves surgical intervention. Opening the compartment(s) by performing a fasciotomy decompresses the compartment and allows for reperfusion of the muscle.
Rhabdomyolysis can result from either direct continued pressure on the muscles or from open crushing injuries.
In a crush injury, the muscle begins to break down and release intravasate debris, such as bone marrow.4 Myoglobin, creatinine phosphokinase (CK) and various inflammatory mediators also are released.
Myoglobin is nephrotoxic at the renal tubular cell level. In a significant crushing injury, where a large area of muscle is injured, myoglobin levels will increase in the serum and also become detectable in the urine. Normal serum myoglobin level is 85 ng/mL or less.
The presence of myoglobin should be suspected whenever the patient's urine appears dark red or brown. A urine sample should be sent to the lab to be checked for red blood cells. If the urine is positive for blood, but negative for red blood cells, myoglobinuria should be suspected. Laboratory testing for myoglobin in both urine and serum should be obtained.
Creatinine phosphokinase (CK) is also released from damaged muscle and soft tissues.5 Myoglobin is cleared from the serum at a much quicker rate than CK, so serum CK levels are more likely to be increased than serum myoglobin levels. The normal CK level is 200 IU. Patients with rhabdomyolysis can have CK levels of 10,000 IU or more. No other disease or medical condition will produce this level of CK elevation, making this a classic diagnostic criterion for rhabdomyolysis.
Acute renal failure may develop in patients with significant crush injuries. At least two factors can contribute to this major complication.
Untreated hypovolemic shock from volume loss or hemorrhage from the crush injury itself or other life- or limb-threatening injuries can precipitate acute tubular necrosis. This "low-flow state" can begin as soon as the patient is injured, and if left untreated can lead to poor organ perfusion. The importance of fluid resuscitation, especially in significant trauma, cannot be overstated.
Potentially toxic circulating myoglobin can worsen already diminished renal perfusion. Again, the need for volume resuscitation in the early stages of injury may decrease the potential of myoglobin-related renal failure.
Fat Embolism Syndrome
Fat embolism syndrome (FES) and acute respiratory distress syndrome may occur from the release of intravasated debris after a crush injury.
FES can occur immediately after injury but generally develops after a latent period of 2-3 days.6 Potentially a quickly fatal syndrome, FES often is associated with crush injuries and long bone fractures.
The fat emboli are believed to cause aggregates that obstruct the pulmonary microvasculature, which in turn causes ventilation perfusion mismatching.6 Generally, the first symptoms are those of acute respiratory failure, including hypoxia and hypercarbia. However, other vague symptoms such as tachycardia and disorientation also may be present. Additionally, the patient may complain of chest pain unrelated to other causes.
Petechia over the chest and neck areas is a highly suspicious symptom of FES, resulting from increased capillary fragility caused by the embolic fat particles.7 Although there is no definitive diagnostic test for FES, an arterial blood gas analysis will show signs of hypoxemia and a chest X-ray will show findings of diffuse pulmonary infiltrates.7 This syndrome likely will produce a situation that warrants immediate and emergent identification and treatment.
Resuscitation and Intervention
As with any trauma patient, the essentials of airway, breathing and circulation must first be addressed. Directing all attention to a mangled or amputated extremity before securing an adequate airway or adequately resuscitating the patient can lead to a potentially fatal outcome. Nothing is gained if attempts are made to salvage an extremity when profound shock or airway compromise produces death in the patient.
Blood loss from soft tissue and musculoskeletal injuries can result in significant problems for the patient. It is essential to identify associated injuries both above and below a crush injury site. Hemorrhage can occur, for example, from a femur or pelvic fracture or any open fracture where blood loss can occur. A tibial fracture can produce a blood loss of up to 750 mL, and a femur fracture up to 1,500 mL.8
Additionally, as mentioned earlier, injured soft tissues produce edema, leading to another source of volume loss from shifts in fluid from the plasma into the extravascular spaces.
Several concurrent interventions must be instituted to ensure adequate resuscitation to both correct significant hemorrhage or blood loss and to prevent life-threatening complications, all focusing on stopping the bleeding and replacing the volume loss.
A physical exam to identify injuries and baseline recordings will be important in order to monitor the patient's response to treatment.8
Intravenous access must be established promptly. This includes either the insertion of two large-caliber (14 or 16 gauge) peripheral intravenous catheters or, if circumstances prevent that route, a large-caliber central venous catheter. Once the intravenous lines are established, blood samples should be drawn for type and crossmatch, arterial blood gas, and any other laboratory tests that may be necessary.
To prevent or reverse the potential for hypothermia in trauma patients, it is important to use warmed fluids. This can be done with a microwave or by storing crystalloid fluid in a fluid warmer. Blood products can be heated with fluid warmers.8
Initially, crystalloid fluids should be used. The appropriate choices of initial fluid resuscitation are normal saline solution or Ringer's lactate solution. These isotonic electrolyte solutions help provide intravascular expansion and replace fluid losses into the intracellular spaces. Although normal saline is an appropriate choice, it has the potential to cause hyperchloremia, especially if the patient has impaired renal function.8
The amount of fluid to administer is often difficult to predict based on the patient's initial presentation.8 The usual volume replacement starts with a fluid bolus of at least 1-2 L for an adult patient and 20 mL/kg for a pediatric patient, given as rapidly as possible.
The patient should be observed during this initial fluid bolus, and further treatment decisions should be based on the patient's response to each therapy. Some patients may respond rapidly to the initial bolus of fluid and require only maintenance fluids. Other patients may respond to the initial fluid bolus but then begin to show signs of inadequate perfusion once the fluids are slowed, signaling either inadequate volume replacement or continued blood loss. Still other patients may not respond at all to the initial fluid bolus or blood administration and may need surgical intervention to determine and correct hemorrhage.8
Blood products may be necessary in patients who sustain crush injuries. As mentioned, fractures can produce large blood loss and quickly lead to a shock state. Whole blood or packed red blood cells can be used to volume resuscitate if the patient does not respond to the initial 1-2 L of crystalloid administration.
Crossmatched blood is preferable; however, the crossmatching process can sometimes take 1 hour. Type-specific blood, usually available within 10 minutes, could provide temporary volume replacement. If type-specific blood is not available, type O packed cells are appropriate for patients who are hemorrhaging.
Verifying Patient Status
A return of seemingly normal vital signs (blood pressure and pulse), does not necessarily indicate normal organ perfusion. Urinary output is a reasonably reliable indicator of renal perfusion and should be monitored closely with an indwelling urinary catheter.
Invasive central venous or Swan-Ganz catheters to determine volume status or cardiac function may be necessary, especially in elderly patients or in patients with a known history of cardiac disease.8 Should this be indicated, the patient will need aggressive monitoring in the intensive care unit.
Depending on the patient's condition, treatment requirements and facility resources, the patient may require a transfer to a specialty or trauma center for a higher level of care or for more definitive care or surgical intervention.
Once initial resuscitation is adequate, rapid assessment and specific interventions can then be directed at tissue preservation. If the patient is to have a successful outcome, treatment goals must be established early and interventions started without delay.
The presence of either an open fracture or a vascular injury must be recognized promptly and treated emergently. Open fractures have a great potential for contamination, leading to problems with healing and function.9 If possible, the extremity should be immobilized and a surgical consultation promptly requested.
Vascular injuries can lead to muscle necrosis within 6 hours.9 Again, immobilization of the extremity and early surgical consultation are necessary to restore arterial or venous flow. Additionally, angiography may be necessary after surgical consultation.9
Generally, most crush injuries will require surgical intervention. Clearly, mangled extremities, degloving-type wounds and amputations need to be thoroughly evaluated and treated, preferably in an operative environment. Prompt effective surgical treatment benefits the whole patient by ameliorating the systemic effects of fractures and related soft tissue injuries by relieving pain and promoting mobilization.4
Certain criteria exist should amputation of an extremity be warranted. For example, criteria for an open tibial fracture include ischemia time greater than 6 hours, and serious associated polytrauma, serious ipsilateral foot injury and requirement for prolonged reconstruction.4
Amputation is a traumatic event for the patient both physically and emotionally.9 Although the potential for replantation should be considered, it must be put into perspective with the patient's other injuries.9 A patient with multiple injuries who requires intensive resuscitation and emergency surgery is not a candidate for replantation.9
As mentioned earlier, compartment syndrome requires a fasciotomy to release the compartment pressures. Staged surgeries are then required to promote healing and for skin grafting.
After sustaining an injury requiring staged surgical interventions or amputation, the patient will need specific goals to meet the challenges of mobility or prolonged disability.
The treatment for rhabdomyolysis is to clear myoglobinuria and prevent acute renal failure. Optimizing renal hemodynamics with prompt and adequate fluid resuscitation, and promoting diuresis with loop diuretics (such as furosemide), is appropriate. Careful monitoring of urinary output with a urinary catheter is needed. Should acute renal failure occur with associated electrolyte abnormalities (such as hyperkalemia), renal replacement therapy may be indicated.5
The treatment for FES is generally focused on quickly identifying the symptoms and providing supportive measures for those symptoms.7 Because this syndrome is potentially fatal, every attempt should be made to improve and support oxygenation and ventilation as early as possible. This would include intubation and mechanical ventilation with positive end-expiratory pressure (PEEP), ongoing respiratory assessments, arterial blood gas analysis and chest X-rays.
Aggressive and appropriate reversal of fluid deficits may be indicated. Again, a pulmonary artery catheter and intensive care monitoring can help manage the patient's fluid status to prevent over- or underhydration.
Finally, potential for significant pain and infection should be considered. Tetanus prophylaxis and antibiotics should be given to treat infection. Open fractures that heal poorly or lead to overwhelming infections may require debridements and hyperbaric oxygen therapy.
Pain management is essential both for the relief of pain and to promote mobilization. Chronic pain associated with prolonged healing or complications may require consultation with a pain management service.
Crush injuries can produce injuries as minor as a laceration that heals in a few days or as severe as a traumatic amputation. Treatment is directed at saving the life first and salvaging the affected extremity or body part when possible.
Following initial interventions, general goals are to maximize functional potential and minimize the risk of complications.
Ellen Plummer is a full partner in the trauma resuscitation unit at the R Adams Cowley Shock Trauma Center, Baltimore. <% footer %>