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Crush Injury

September 3, 2022 - read ≈ 17 min



Brittany L Powell, MD

Department of Surgery, Brigham and Women’s Hospital, Boston, MA


Christopher J Burns, MD

Department of Surgery, South Shore Hospital, Weymouth, MA and Department of Surgery, Brigham and Women’s Hospital, Boston, MA



Crush injury is caused by the static compression of body parts causing localized damage to skeletal muscle and nerves, most commonly involving the lower extremities[1-3]. Skeletal muscle can withstand 2 hours of ischemia without permanent injury, 2-4 hours with some reversible cell damage, and may suffer irreversible necrosis by 6 hours of ischemia time [4]. However, muscle and nerve damage can also occur during the initial mechanical injury, in addition to tissue loss in the period of ischemia and subsequent reperfusion [1,5].

Crush syndrome is the resultant systemic sequelae of local crush injury [3]. This is typically seen in crush injury to the limbs, because the impact needed to cause this crush syndrome on the torso or head is thought to be too much force to survive [1,6].

When muscle cells do not receive oxygen due to the compression of the venous (and arterial) systems, cell damage occurs and toxic muscle cell breakdown products accumulate in the injured tissue. When the crushing force is relieved and blood supply is restored, these toxic byproducts circulate systemically. This release back into circulation can cause multiple electrolyte abnormalities, toxicities, and physiologic abnormalities, including: metabolic acidosis, hyperkalemia, hypocalcemia, acute renal failure, hypovolemic shock, acute cardiomyopathy, disseminated intravascular coagulation, and hypothermia [7].

Clinical Presentation

Torso crush injuries

Thoracic crush injuries can lead to death through multiple mechanisms – hemopneumothorax, aortic transection, pericardial tamponade, cardiac contusion, rib fractures, flail chest, lung contusion, or traumatic asphyxia [8,9].

Abdominal crush injuries can cause immediate catastrophic damage to solid abdominal organs, can cause an aortic tear or rupture, and can cause retroperitoneal bleeding. Crush injuries that cause failure of more than one organ system are often fatal, especially if rescue is delayed [1,10].

Limb crush injuries

These injuries are often survivable even with multiple fractures, large open wounds, and/or multiple amputations [1]. For patients found with a crush injury to limbs, there can be many falsely reassuring signs as conscious patients rarely complain of pain, their vital signs are frequently near to (or actually) normal, and they almost universally have good pulses due to infrequent direct injury to arteries. In addition, their limbs are rarely swollen, they might complain of only patchy numbness, and their skin is usually surprisingly intact, yet may be ecchymotic [1].

Pelvic crush injuries

Pelvic crush injuries can lead to death by exsanguination. If patients survive the initial injury, they are at risk of sepsis and multi-organ failure [1,11,12]. There should be a high clinical suspicion for concomitant rectal and/or urethral injuries [1,13,14].

Head crush injuries

These injuries often lead to instant death, which can involve skull fracture, increased intracranial pressure, and brain parenchymal injury [1].

Less severe crush injuries should be triaged emergently as their timely management is imperative to potential survival. Major crush injuries, or crush injuries to the head, are often considered futile [3].


Extrication for crush injury patients can be a prolonged process. A hallmark of crush injury management is to begin resuscitation while the limb or body part is still trapped. This dilutes the toxic byproducts of devitalized muscle tissue when they are released into systemic circulation upon removal of the crushing force.

Crystalloid fluid resuscitation should be initiated at a rate of 0.5-1.5L/hr via intravenous or intraosseous access prior to removing the crushing object, especially for prolonged crush >4 hours (or if the patient is found to have an abnormal vascular or neurologic exam).

Ringers Lactate should be avoided, since it contains a very small amount of potassium. The patient should receive an initial resuscitation of 1-2L of normal saline before removal of the crushing force to prevent hypovolemic shock, pulmonary embolism, and/or hyperkalemic/hypocalcemic cardiomyopathy [15,16].

If it is not possible to initiate fluid resuscitation immediately, a tourniquet should be placed to maintain compression until fluid resuscitation can be initiated to avoid rapid deterioration which could possibly lead to death. It is important to note that application of a tourniquet for a prolonged period can cause rhabdomyolysis, permanent neurovascular damage and skin necrosis [17], and it should be removed as soon as resuscitation can be started and/or the patient can be transferred to definitive medical care, ideally with dialysis capability [1]. See Figure 1 [22].

Figure 1. Fluid administration algorithm for adults before and during extrication for crush injury
Reprinted with permission from Sever MS, Vanholder R, RDRTF of ISN Work Group on Recommendations for the Management of Crush Victims in Mass Disasters. Recommendations for the management of crush victims in mass disasters. Nephrol Dial Transplant 2012; 27 (Suppl 1):i1. (22)

Continuous cardiac monitoring and urine output monitoring should be initiated as soon as possible. Within 1-2 hours of the body part being released from the compressive force, hyperkalemia, hypocalcemia, and oliguria will serve as early clinical signs of crush syndrome, and might precipitate cardiac arrhythmias and cardiac arrest [18]. Serial potassium measurement should be sent every 3-4 hours during the acute management of the crush injury (i.e. the first 3-4 days), if possible. Most early deaths are due to hyperkalemia or hypovolemia [6,19].

Myoglobin has a short half-life (3hr) and is filtered in the kidney, so blood myoglobin production and urine myoglobin clearance can be monitored and compared to trend the course of crush syndrome [7]. CK levels >5000 U/L is associated with the development of Acute Kidney Injury [20].

Fluid resuscitation should continue until there is clinical and biochemical resolution of myoglobinuria, usually about 3 days after injury [15,21,22]. The rate of infusion should be guided by clinical response. Isotonic saline is the first choice for fluid during resuscitation. See Figure 2 [22], an algorithm to guide post-extrication resuscitation. Blood products may needed to treat dilutional anemia, and should be administered with Plasma, red blood cells (RBCs), and platelets in a balanced ratio.

Figure 2. Algorithm for ongoing fluid resuscitation after extrication
Abbreviations: IV, intravenous; L, liters
Reprinted with permission from Sever MS, Vanholder R, RDRTF of ISN Work Group on Recommendations for the Management of Crush Victims in Mass Disasters. Recommendations for the management of crush victims in mass disasters. Nephrol Dial Transplant 2012; 27 (Suppl 1):i1. [22]

Hyperkalemia can be treated in a three-part approach to [1] stabilize the myocardial cell membrane, [2] shift the potassium intracellularly, and [3] assist with potassium excretion.  Calcium gluconate or calcium chloride should be administered for cardiac membrane stabilization.

Insulin (and added glucose to prevent hypoglycemia), sodium bicarbonate, and nebulized albuterol redistribute the potassium from extracellular fluid to inside the cells. And finally, potassium binders (sodium polystyrene sulfonate/Kayexalate at 15g per day per patient), furosemide, and hemodialysis assist with the patient’s actual potassium excretion

Nephrologists should be involved in care early to help assess the need for dialysis, if that service is available. It is also important to correct compounding conditions of hypothermia, acidosis, and coagulopathy. Patients with this “lethal triad of trauma” have an even higher mortality rate [1,23]. Rewarming with warmed IV fluids, warm air blankets, heat lamps, heated respiratory gases, bladder lavage, and warm enemas should be aggressively implemented as able and tolerated [24].

The process of reperfusion is extremely painful and distressing and should be treated with analgesics and anxiolytics, including opiates, ketamine, benzodiazepines, and Entonox (oxygen and nitrous oxide), as needed [16,17,25].

Operative/Postoperative management

Field amputations of crushed limbs should be a last resort, but may be deemed necessary if the trapped limb is preventing extrication. If an amputation is deemed necessary, it should be performed as distal as possible. Limb amputation before release of the crushing force, similar to tourniquet application, may prevent some of the sequelae of reperfusion injury [27,28].



Rhabdomyolysis leads to electrolyte and mineral disturbances, myoglobinuria, oliguria, and hypovolemia [1,29]. Rhabdomyolysis can be diagnosed with serum creatinine kinase (CK) > 1000 U/L or five times upper limit of normal [1]. Rhabdomyolysis should also be a concern for patients who are found down for an unknown period of time [16].

Myoglobin leads to obstructive renal failure with clinical sign of “tea-colored” urine [28]. Fluid resuscitation, electrolyte correction, and supportive critical care, in severe cases intermittent hemodialysis, are the mainstays of treatment for rhabdomyolysis [29].

Compartment syndrome

Hours after extrication, limbs will begin to swell. Lack of venous outflow or arterial inflow for 4-6 hours, and arterial and venous injury in combination (especially the popliteal artery and vein), can put a patient at a very high risk for developing compartment syndrome [30].

Compartment pressures can be measured using a Stryker Intra-Compartmental Pressure Monitor System (Stryker Instruments, Kalamazoo, MI), but usually compartment syndrome is a diagnosis based on phyiscal exam [30]. For absolute pressures of 30-35 mmHg, a fasciotomy should be performed. In the absence of a Stryker needle, clinical judgement should be used to determine the liberal need for an emergent fasciotomy.

Other clinical signs and symptoms of compartment syndrome include severe progressive pain often “out of proportion” to the clinical situation, and firmness and decreased compressibility of compartments. Paresthesia develops later, while paralysis and pulselessness are considered late findings of compartment syndrome [31], and indicate a dire clinical diagnosis. Patients may have nerve damage and therefore may actually have an absence of severe pain, or may be sedated and unable to report pain, so maintaining vigilance for the development of compartment syndrome is imperative, and early aggressive intervention must be considered. Fasciotomy guidance can be found in Figure 3-19, shared with permission, all medical illustrations by Ms. Elizabeth Weissbrod, MA, CMI [32].

Figure 3. The volar incision as seen on the right arm enabling decompression of the anterior (volar) and mobile wad compartments.
Figure 4. The dorsal incision as seen on the right arm with additional incisions on the hand enabling decompression of the dorsal compartment of the forearm and the intraosseous compartments of the hand. 
Figure 5. The median nerve (star) is identified at the wrist crease running under the palmaris longus (PL) tendon. Scissors are placed above and below the transverse carpal ligament (arrow) which is divided to completely open the carpal tunnel.
Figure 6. The cross-sectional anatomy of the mid-portion of the left lower leg depicting the four compartments that must be released when performing a lower leg fasciotomy.
Figure 7. The fibular head and lateral malleolus (on the right lower leg) are reference points to mark the edge of the fibula and the lateral incision (dotted line) is marked one finger in front of this (A FINGER IN FRONT OF THE FIBULA).
Figure 8. The medial incision (dotted line) is marked (on the medial left lower extremity) one thumb breadth below the palpable medial edge of the tibia (solid line). A TUMB BEHIND THE TIBIA.
Figure 9. The lateral incision on a right lower extremity demonstrates the intermuscular septum (dotted line), which separates the anterior and lateral compartments of the lower leg. Note one of the perforating vessels (arrow) which enters and helps to identify the septum
Figure 10. The fascia of the right lateral lower leg (foot to the right) is opened in a classic “H”-shaped fashion for the length of the compartments with scissors turned away from the septum to avoid damage to underlying structures as seen on the right.
Figure 11. The superficial peroneal (fibular) nerve (arrows) runs in the lateral compartment from the knee and crosses over the septum (star) into the anterior compartment 2/3 to 3/4 of the way down the leg towards the ankle. This must be carefully avoided by keeping the scissor tips pointed away from the septum and looking for the nerve as the fasciotomy is extended to the lateral malleolus. The left lateral lower leg is seen on the left and the right lateral lower leg is seen on the right.
Figure 12. There is an intermuscular septum (red arrow) between the lateral and superficial posterior (post) compartments which can be mistaken for the septum between the anterior and lateral compartments (blue arrow) if the incision is made too far posteriorly.
Figure 13. If the lateral incision is made too far posteriorly the intermuscular septum (red arrow) between the lateral (L) and superficial posterior (SP) compartments can be mistaken for the septum (blue arrow) between the anterior (A) and lateral (L) compartments with the anterior missed.
Figure 14. The medial incision as seen on the left lower leg is placed such that the saphenous vein can be identified and preserved and the fascia (star) is opened to expose the soleus and gastrocnemius muscles in the superficial posterior compartment. The superficial posterior compartment is exposed by opening the superficial fascia (star) below the edge of the tibia (arrows)
Figure 15. On the left medial lower leg the soleus muscle (stars) is dissected off of the inferior border of the tibia (arrow) allowing entry into the deep posterior compartment.  
Figure 16. Identification of the posterior tibial neurovascular structures (arrows) confirms entry into the deep posterior compartment after taking the soleus muscle down from the tibia as seen on the left (picture to left) and right (picture to right) medial lower leg..
Figure 17. If the dissection plane is made between the soleus (S) and gastrocnemius (G) muscles, the deep posterior (DP) compartment has not been opened and the soleus fibers must be taken down from the underside of the tibia (star) to separate the superficial posterior (SP) from the deep posterior compartment such that it can be opened.
Figure 18. The plantaris tendon (arrow) is found in the plane between the soleus and gastrocnemius muscles and may be mistaken for the posterior tibia neurovascular bundle. In order to enter and decompress the deep posterior compartment the soleus muscle must be taken down from the underside of the tibia.
Figure 19. The three compartments of the thigh are Anterior (purple), Medial (orange), and Posterior (green).The two incisions required to decompress the compartments of the thigh are depicted with the anterior (purple) and posterior (green) compartments opened via the lateral incision and if indicated the medial (orange) compartment opened through the medial incision.

Reperfusion injury

When pressure is suddenly released in a crushed limb, acute hypovolemia and metabolic abnormalities can ensue. Reperfusion injury, especially during fluid resuscitation can lead to compartment syndrome. It can also lead to patient death. Reperfusion of limbs can cause sudden release of bone marrow, fat, and thrombus, leading to pulmonary embolism, stroke, and/or fat emboli syndrome. It is important to note any clinical changes in respiratory or neurologic status during and after reperfusion [1,31].


In their longer-term recovery, crush injury patients should be considered immunocompromised due to an acute kidney injury and their catabolic state, and are susceptible to developing overwhelming sepsis. They will have many possible infectious sources, which should be meticulously monitored, in alignment with critical care guidance [1,34].


  • Prolonged crush injury can lead to crush syndrome, the systemic sequelae that results when the breakdown products of dead skeletal muscle cells are released upon restoring circulation and reperfusion of the limb or body part. This can lead to hyperkalemia, hypocalcemia, metabolic acidosis, hypovolemic shock, and other downstream effects.
  • Aggressive early fluid resuscitation, preferably initiated before extrication, and supportive critical care are the hallmarks of management in crush injury.
  • There are many serious complications that can arise from crush injury including rhabdomyolysis, compartment syndrome, reperfusion injury, and sepsis. Clinical vigilance during the resuscitation and recovery phases of care and aggressive interventions are imperative to minimizing morbidity and mortality.


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