Crush syndrome

Dario Gonzalez, MD, FACEP

The assessment, management, and treatment of the entrapped victim are critical skills needed to ensure a successful outcome. Individuals have been trapped in the rubble for even short periods of time only to succumb to predictable consequences of muscle compression injury. The clinician should be prepared to address issues of crush syndrome (including compartment syndrome) proactively and aggressively. The history of this disease is clear and well documented both in the military literature and in the earthquake rescue reviews. The key to management is managing and predicting arly 20th century reports have described a clinical group, sometimes seen in association with disasters, of muscle injury, renal failure, and death. This included manmade (i.e., war) and natural (i.e., earthquake) events. Earthquakes are estimated to have a 3% to 20% incidence of crushing injuries (1). The collapse of a multistory building may cause crush injury in up to 40% of the extricated survivors (2). This number becomes more relevant today in the advent of terrorist bombings. The earliest modern reports (1910) of rhabdomyolysis appear in German literature and, at that time, the classic triad of a syndrome (Myer Betz) of muscle pain, weakness, and brown urine. The World War I medical literature described situations in which similar signs and symptoms were seen in German soldiers who were buried and rescued from trenches. At the time of the London Blitz, Bywaters described a frequently seen constellation of signs and symptoms in trapped Blitz survivors. Dr. Bywaters, a nephrologist, was the rst to use the term crush injury for this condition. He also discovered the cause of this condi1

clinical conditions before they present themselves. The potential exists in the urban environment (with the potential of building collapses) to have patients with crush syndrome that far exceed local medical capabilities should be part of modern disaster planning. This article reviews the various body systems and presents management and assessment strategies for the clinician. (Crit Care Med 2005; 33[Suppl.]:S34 S41) KEY WORDS: crush syndrome; acute renal failure; rhabdomyolysis; earthquake; building collapse; conned space

From Fire Department City of New York, Ofce of Medical Affairs; Emergency Department Long Island Jewish Hospital Center, New Hyde Park, NY; Urban Search and Rescue, New York Task Force DNE. Copyright 2005 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins DOI: 10.1097/01.CCM.0000151065.13564.6F

tion to be rhabdomyolysis. In May 1941, during the London Bombings (Battle of Britain), he conducted a study of four young healthy patients trapped in building rubble for 3 to 4 hrs. All had limbs crushed but survived the initial rescue, extrication, and hospital transport. They all developed the symptom complex of shock, swollen extremities, and dark urine. The patients survived the initial shock but progressed to renal failure. All died of uremia days later. Renal biopsy demonstrated . . .in the renal tubules, degenerative changes and casts containing brown pigment (3). Dr. Bywaters correctly identied the etiology as muscle necrosis. He described all these individuals who were successfully extricated (from the bombings) who subsequently died. All had oliguria, pigmented casts, limb edema, associated shock, and death. Amongst air-raid casualties seen at this hospital have been four cases of crush injury. . .. The patient had been buried for several hours with pressure on the limb. On admission he looked good except for swelling of the limb, some local anesthesia and whealing. A few hours later the blood pressure falls. This is restored to preshock levels by transfusions of serum, plasma or, occasionally blood. The urinary output, initially small, diminishes further. The urine contains albumin and many dark brown or black granular casts. Slight generalized edema, thirst and incessant vomiting develop. The blood urea and potassium, raised at an early stage, become progressively

higher and death occurs comparatively suddenly, frequently within a week (4). In 1943, Bywaters and Stead used an animal model (rabbit) to identify the offending agent as myoglobin, also known as rhabdomyolysis. Dr. Bywaters recommended an alkaline rehydration to prevent the complications of the traumatic rhabdomyolysis. His treatment plan consisted of restoring urinary output by heat to the loins; saline dilution; increasing blood volume (hence blood pressure) and the use of diuretics (caffeine), without the use of early amputations (a common approach at that time). The condition and rate of acute renal failure (ARF) continued as part of historical military experience. In World War II, 91% mortality was attributed to prolonged evacuation time. In the Korean Conict, there was a documented 84% mortality rate predialysis. This decreased to 53% mortality once dialysis was introduced and available. In the Vietnam War, there was 50% mortality; this was attributed to shorter evacuation times. Today, the primary management of the entrapped victim is early uid administration with unied and coordinated victim extrication. Early hydration has been demonstrated by Better and colleagues, from Israel building collapses, 1979 and 1982, to positively affect victim survival. In 1979, intravenous uids were administered postextrication with a mean delay of 12 hrs. The net result was that seven of seven survivors developed ARF. In 1982, the procedure in place allowed
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for the administration of intravenous uids during extrication. The net result was that one of eight developed ARF. He concluded that to prevent systemic and renal complications, early and vigorous uid resuscitation was needed. The uid administration should begin at the incident location (entrapment site) before extrication is accomplished. On July 28, 1976, a magnitude 7.8 earthquake struck the ancient city of Tangshan (near Beijing). There was a total of 350,300 injuries and 242,769 deaths, approximately 20% from crush syndrome. Modern-day earthquakes have struck the following locations: Spitak, Armenia, 1988; Hanshin, Japan, 1995; and Marmara, Turkey, 1999. The 1988 6.9 Richter Scale earthquake of Spitak, Armenia, resulted in the death of 50,000 people and 600 cases of ARF that required hemodialysis. There were three common factors to all the events. They were the lack of sufcient local emergency resources, poor rescue and medical coordination, and lack of equipment. Lessons from Armenia directly impact on the medical management of entrapped victims that present to this very day for continued in-hospital critical care. That is the need to proactively address the issue of rhabdomyolysis and its associated complication of ARF. In Armenia, dialysis machines were not readily available; this resulted in dialysis machine triage. Even with this, many patients had to be transported to gain access to dialysis machines, which further complicated their clinical course. A group of British nephrologists identied the need for a permanent relief team to deal with the issue of renal care. This was created in 1995 and became known as the Disaster Relief Task Force. Their ultimate goal was to treat and prevent ARF from traumatic injuries. The earthquake of Hanshin, Japan, in 1995, 7.2 on the Richter Scale, produced 5,500 fatalities and 372 crushed injury victims. From this group, 202 developed ARF and 78 required hemodialysis. This number of cases was a direct result of the delay in initiating aggressive medical care, not necessarily delays in extrication. The Marmara, Turkey, earthquake of 1999 was a 7.4 Richter Scale event. The European branch of the Disaster Relief Task Force was dispatched to the earthquake site within 6 hrs. There were 462 cases of ARF with an associated fatality rate of 19%. This signicant improvement was attributed to the early availability of portable dialysis machines.
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The Conned Space Rescue

To appreciate the medical complications associated with crush syndrome (also known as traumatic rhabdomyolysis), it is important to understand the operational factors associated with this entity. Conned space medicine should be considered a subset of conned space rescue rather than a pure medical entity. It is one of the few areas of medicine that is interlinked and dependent on the actions (or lack of) nonmedical personnel. It is only through many incidents that the prehospital physician rescue group has intertwined themselves in mechanical rescue process. The traditional rescue view is to extricate and evacuate to medical sources before medical care can be initiated (despite the outcome). Within the rescue community, the extrication of a live victim is considered a success. Conned space rescue of victims involved in situations where there is a conned space, which is dened by the Occupational Safety and Health Administration (OSHA) as a location(s) where there is limited or restricted entry or exit. The typical location is not designed for continuous safe occupancy; such locations include underground vaults, silos, septic tanks, storage tanks, sewers, etc. Conned spaces are particularly hazardous as a result of the presence of a variety of inherent dangers such as a hazardous toxic atmosphere (i.e., carbon monoxide), the physical potential for engulng the entrant (i.e., trench collapse), and potential asphyxiation (i.e., low oxygen environment). The conned space rescue is a dangerous undertaking as a result of the immediate (and delayed) life safety issues and therefore accounts for the extended rescue to denitive medical care time (time of arrival to an appropriate healthcare facility). The environment is considered so dangerous that traditionally medical care was deemed as inappropriate in the hole. One study conducted revealed that 1.6 rescuers died for every initial victim rescue. Potential hazards in conned spaces can include: poor air quality, suspended pollutants, toxic gases, an explosive/ ammable atmosphere, and insufcient oxygen concentration. Biologic hazards such as sewage or body parts or uids may affect the rescuer and/or the victim. All of these were seen in the 2001 collapse of the World Trade Towers. All of these hazards must be considered by the critical care clinician when assessing or

managing a rescue survivor. The indirect insults may account for the pulmonary compromise, unexplained secondary infection, renal and cardiovascular impairment.

Crush Syndrome
Crush syndrome results in a characteristic syndrome of rhabdomyolysis, inducing myoglobinuric ARF, also known as traumatic rhabdomyolysis. Crush syndrome is fundamentally based on three criteria: 1. Involvement of muscle mass; 2. Prolonged compression (usually 4 6 hrs, but possibly 1 hr); and 3. Compromised local circulation. The total entrapment time (time under rubble plus removal from the site) may not reect the true severity of injury or the potential medical complications. Renal and cardiac complications are particularly sensitive to the magnitude of pressure and size of the compressed muscle groups (with respect to overall compression time). Entrapment with muscle trauma can lead to compartment syndrome or traumatic rhabdomyolysis. The rhabdomyolysis under these circumstances is potentially a fatal outcome. Crush syndrome (also known as traumatic rhabdomyolysis) results from muscle reperfusion with subsequent secondary systemic effects. These are all direct and indirect consequences of prolonged, continuous pressure on the limbs. The destruction of muscle tissue and the inux of myoglobin, potassium, and phosphorus into the circulation results in the classic picture of traumatic rhabdomyolysis/crush syndrome. The syndrome is characterized by hypovolemic shock and hyperkalemia. This is seen in natural and other types of disasters such as earthquakes, war settings, vehicular accidents, and events involving pinning under heavy objects. The same consequence can be seen if the victim is unable to move (i.e., coma or the drug overdose setting) and reduce or relieve the compression forces on the muscle group. The most important prehospital goal is to remove compressive forces and hydrate as soon as possible. The clinical presentation of crush syndrome is rst based on history of the event and a high index of suspicion. Compression 1 hr is likely to result in a crush syndrome, but this has been seen in as little as 20 mins. The clinician should evaluate the physical presence of
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skin trauma or local signs of compression (erythema, ecchymosis, bullae, abrasion, etc) on a muscle mass. The absence of a pulse or a weak, thready pulse to the distal limb may be an indicator of muscle swelling or compromised circulation. Continued assessment may demonstrate a pale, cool, diaphoretic limb, which may be anesthetic. Crush syndrome results from lysis of skeletal muscle cells and the subsequent compromise of cell wall integrity and leakage of cellular contents. In normal muscle physiology, the intracellular environment is maintained by the Na/K ATPase such that there is a low concentration of Na and a high concentration of Ca . The mechanical stress opens Ca channels with an inux of Na , Ca , uid, and neutrophils. The cellular effects of crush syndrome include interference of Na/K ATPase, intracellular calcium inux, cell edema, dysfunction, and death. All of these essentially result from the leakage of myoglobin, creatine kinase, potassium, and calcium into the circulation. These patients have classically been described as presenting with muscle weakness, malaise, and fever. This underestimates the real danger that lies in cardiovascular effect as a result of electrolyte imbalance and renal failure. This is exclusive of the associated direct muscle trauma, i.e., crush injuries of the extremities, pelvis, or head. Crush syndrome may be exacerbated by hypovolemia secondary to sequestered uids or frank hemorrhage. It is possible for muscle compartments to sequester up to 12 L of uid in a 48-hr period.

nitrogen ( 40 mg/dL), serum creatinine ( 2 mg/dL), uric acid ( 8 mg/dL), potassium ( 6 mg/dL), or phosphorus ( 8 mg/dL) and a decreased serum calcium ( 8 mg/dL).

Pathophysiology
Crush syndrome is caused by disruption of adequate tissue perfusion of an affected muscle group. The mechanisms of injury may include direct muscular trauma, blunt or penetrating trauma, or extended muscle pressures. Microvascular trauma from prolonged application of a compressive force ultimately leads to cellular hypoperfusion and/or hypoxia. Hemorrhage from torn or compressed vessels can impair blood ow and oxygen delivery to tissues. Bleeding into an intact compartment may also lead to a compartment syndrome situation with decreased perfusion and local neurovascular dysfunction. Microvascular trauma can lead to extracellular edema and the progression to compartment syndrome. Resulting hemorrhage, edema, and hypoperfusion combine to cause tissue hypoxia and ischemia. The capillary blood ow can be affected at pressures as low as 20 mm Hg with subsequent hypoxic injury from decreased oxygen tension. Metabolic abnormalities occur when the decreased perfusion and subsequent hypoxia results in a decrease of available adenosine triphosphate (ATP). This is compounded by the eventual cellular acidosis. Less ATP causes failure of Na-K ATPase pump and sarcolemma leakage. Lysed cells release inammatory mediators that cause platelet aggregation, vasoconstriction, and vascular permeability leading to further edema and decreased tissue perfusion. Potassium, phosphate, purines, lactic acid, thromboplastin, creatine kinase, and myoglobulin are also released from lysed cell. Metabolic abnormalities result in hypovolemic shock, hyperkalemia, metabolic acidosis, compartment syndrome, and ARF. The crushing of the entrapped muscle for as little as 2.5 hrs may result in irreversible ischemic muscle necrosis. When rescued and extricated, blood ow to the ischemic limb is reestablished, allowing perfused uids to become entrapped in damaged tissue, resulting in edema, hemoconcentration, and clinical shock. Some of the uids perfusing the necrotic muscle reappears in the venous drainage, along with other protein components, allowing large quantities of myoglobin, potassium, and

Diagnostic Criteria
Compression injury to a large mass of skeletal muscle produces both microscopic and macroscopic injury. Compressed limbs eventually become tense and edematous with compromised vascular circulation. The secondary sensory and motor disturbances in the compressed limbs are commonly seen. The microscopic consequences are local until revascularization occurs. Laboratory evaluation requires the clinician to monitor the urine myoglobin, serum creatine phosphokinase, and serum electrolytes. The revascularization of ischemic tissue has systemic consequences. This results in myoglobinuria and/or hematuria. There may be seen peak creatine kinase 10,000 U/L, oliguria (urine output 400 mL/24 hrs), elevated blood urea
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phosphorus to enter the venous circulation. The myoglobin released into plasma is readily ltered by the glomerulus, which transiently appears in the urine as pigmented casts. Volume depletion, along with release of acid components from injured muscle, causes a drop in urine pH. The low urine pH causes myoglobin to form a gel, which obstructs the distal nephron, resulting in oliguria. Potassium disrupts cardiac rhythm and calcium precipitates in injured muscle, causing a potentially lethal combination of hypocalcemia and hyperkalemia. Oliguria, anuria, hyperkalemia, and uremia become overt and lead to death in 37 days. Autopsy shows kidneys that are overweight and edematous with areas of infarction. Distal tubules show occluding casts containing myoglobin. More proximal tubules in the nephron show varying degrees of tubular injury or necrosis. Treatment is directed toward early aggressive hydration and forced diuresis. Trapped victims should have had resuscitation initiated before extraction where possible. Normal saline is the usual crystalloid given to achieve urine an output of 100 200 mL/hr. The addition of agents to alkalinize the urine has been shown to improve clearance of myoglobin and prevent or decrease precipitation of myoglobin. Fluid requirements may be signicant such that it is possible to sequester (third space) in the crushed area 12 L of uid over a 48-hr period. If inadequately corrected, this potentially fatal hypovolemia may cause renal ischemia by activating secretion of constrictor hormones such as angiotensin II, catecholamines, vasopressin, and intrarenal thromboxane. Alkalinization of urine is critical to control or minimize heme cast deposition. The uses of sodium bicarbonate and acetazolamide have been advocated in this setting. Early surgical therapy is not indicated, but rather a delayed approach to debridement of any necrotic tissue is warranted. Medical therapy includes the use of mannitol, allopurinol, benzamil, and amiloride.

The Renal Effects of Crush Syndrome

The microvascular effects of muscle crush injury result in traumatic rhabdomyolysis or crush syndrome. The systemic manifestations of crush syndrome are electrolyte abnormalities, metabolic acidosis, hypovolemia, disseminated inCrit Care Med 2005 Vol. 33, No. 1 (Suppl.)

travascular coagulation, and ARF. In these circumstances, up to 40% of patients with rhabdomyolysis will develop ARF. The pathophysiology of ARF in crush syndrome is some effects of interconnected renal insults. This includes the obstructing intratubular heme pigment cast. These cast deposits result in proximal tubular cell injury that is mediated by free chelatable iron and by the heme center of myoglobin with resulting renal ischemia. Cast formation leads to tubular obstruction and myoglobin nephrotoxicity causing renal vasoconstriction. The level of creatine phosphokinase is the most sensitive indicator of the extent of muscle injury. Serum creatine phosphokinase 20,000 requires treatment and critical care monitoring. After the Kobe, Japan, earthquake, some rescued victims were found to have levels 75,000. Add to these intrarenal effects of systemic volume depletion and associated renal ischemia. The diagnosis may be initially based on a history of crushing injury. In the event of a comatose or obtunded patient, this may only be documented on the prehospital provider ambulance run sheet. Clues to the presence of acute traumatic ischemia (ATI) may be assumed by the mechanisms of injury, history of prolonged immobilization, a history consistent with a crush mechanism, or in a conscious patient pain out of proportion to the apparent extent of injury. Laboratory ndings in rhabdomyolysis and ARF may be seen by the elevation of creatine kinase typically greater than 10,000 IU/L. The creatine kinase level is the most sensitive indicator of crush syndrome. The patient may present with what appears to be hematuria but is rather myoglobinuria, or the urine may appear to have a color change to reddishbrown. Urinalysis may demonstrate pigmented granular casts in urine. Serum analysis may demonstrate hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. Additionally, there will be a rise in serum creatinine. Prevention and treatment in the prehospital sector may include standard trauma protocols, oxygen, cardiac monitoring, removal of restrictive clothing or jewelry, and possibly eld amputation. Three major modalities to prevent or minimize the severity of ARF in this setting are intravenous uid hydration, alkalinization, and, under special circumstances, forced diuresis. Intravenous
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uids can be started before the crush is relieved and therefore before a signicant amount of heme pigment has been released into central circulation. Initial uid resuscitation should begin with 250 mL bolus normal saline (0.9% NS) every 15 mins until urine is produced at a rate of 2 mL/kg per hour. If aggressive uid resuscitation is started after the rst 6 to 12 hrs, it may be ineffective and may simply lead to uid overload. There is no clear evidence of benet of other uids (Ringers lactate) over normal saline. These may precipitate alkalosis, precipitation of calcium phosphate, and hypocalcemia. Once the patient is hemodynamically stable, intravenous uids can be switched to 1/2 NS with 40 mEq sodium bicarbonate for alkalinization of urine. The purpose of sodium bicarbonate is to raise the urine pH to 6.5 and diminish myoglobin renal toxicity by increasing the solubility of heme pigments. Solubility of myoglobin in urine (5) using 50 mg myoglobin/mL urine is summarized in Table 1. Acetazolamide, a carbonic anhydrase inhibitor, may be useful if pH is 7.5 after bicarbonate therapy or aciduria persists despite alkalemia. Acetazolamide will correct metabolic alkalosis and increase the urine pH. A danger associated with the metabolic alkalosis is metastatic calcication; however, this danger is outweighed by the hypokalemic action of the treatment and by the production of alkaline urine, which prevents renal damage from myoglobin. Forced diuresis may be accomplished by the use of Lasix (40 120 mg intravenously) or Mannitol (1.52 g/kg intravenously as a 20% solution). It is believed that Lasix (furosemide) can help by causing renal vasodilatation, decreased renal oxygen demands, and increased renal intratubular ow. Loop diuretics have a theoretical disadvantage of acidifying the urine; however, this is outweighed by the signicant volume of urine created. Mannitol works as an osmotic diuretic and volume expander. However, it may lead to volume overload and an osmolar gap. The administration of calcium gluconate or calcium chloride for the treatment of severe hyperkalemia should be undertaken with caution as a result of the potential hyperkalemicinduced arrhythmias. Calcium administration is indicated only in the presence of electrocardiographic changes secondary to hypocalcemia or hyperkalemia. Patients should be managed in a hemodialysis-capable facility, although serum

Table 1. Solubility Urine pH 8.5 6.5 5.5 5.0 5.0 Percent Precipitated 7.50 4 23 46 73

myoglobin levels are not reduced by hemodialysis. The combination of glucose and insulin are a known intervention for the management of hyperkalemia. In the case of crush syndrome, this treatment modality may not induce cellular uptake of potassium. This requires the physician to use alternate modalities to lower potassium. Crush injury has a signicant toxic kidney effect. Damage to the kidney occurs by obstruction of tubules by casts, hypovolemia, and damage of renal tubular cells by heme complexes. Early and aggressive uid hydration for crush syndrome is paramount. Goal-directed therapy is to achieve a urine output of 200 300 mL/hr at a pH between 6 and 7 (keep serum pH below 7.50). At the same time, it is important to achieve hemodynamic stability and prevent volume overload. In the Spitak, Armenia, earthquake of 1998, approximately 50,000 deaths occurred and 600 individuals required hemodialysis for ARF. In the Kobe, Japan, earthquake of 1995, 6,000 deaths occurred and 6,107 patients were hospitalized after the earthquake; 372 presented with crush syndrome, with a mortality rate about twice that of other trauma patients. In an environment of limited resources, the solution to the renal complications is prevent or minimize the incidence of ARF.

Cardiovascular Effects
The cardiovascular pathophysiology is the results in hypovolemia, shock, hyperkalemia, hypocalcemia, acidemia (lactate), and hyperphosphatemia. The systemic effects of hypovolemia, the direct effects of electrolytes, and associated toxin releases are cardiotoxic. Animal studies (rabbit) and clinical experience demonstrate that hypovolemic shock can be induced with crush syndrome. Large volumes of intravascular uid can be sequestered in the involved extremities secondary to the increased capillary permeability. Oda conrmed that hypovolemic shock was the most
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common cause of death after crush injury (23 of 35, 66%) in the rst 4 days. Hypovolemia can result when large amounts of uid are absorbed by crushed muscle. Fluid sequestration presents itself in the clinical picture of hypovolemic shock. Hypovolemia can potentiate the renal failure and cardiac instability of crush syndrome. In large injuries, a patient can third space the circulating volume of a 75-kg person. Fluid replacement within 6 hrs postinjury is imperative to prevent hypovolemia and acute tubular necrosis. Cardiovascular complications are associated with arrhythmias secondary to the hyperkalemia and the associated acidosis. Both make the heart susceptible to cardiac arrhythmias. Simultaneous electrolyte abnormalities may also include hypocalcemia and hyperphosphatemia. Hyperkalemia and its associated cardiotoxicity represent the second most common cause of early deaths after crush injury from the potassium released, from damaged cells, into the circulation. The effects of potassium are the result of cell membrane dysfunction allowing the leakage of intracellular potassium. Hyperkalemia at levels 6 mg/dL causes cardiotoxicity. The largest amounts of potassium are stored in skeletal muscle. When released, the kidney is unable to excrete large loads of potassium even with normal renal function. The additional additive effect of dehydration, uid third spacing, and release of cellular potassium may cause arrest within 1 hr after removal of compressive forces. The cardiovascular effects can be signicant and result in substantial morbidity and mortality. The metabolic effects on cardiovascular system are primarily associated with electrolyte imbalance and hypoperfusion. The leakage of phosphate from lysed cells results in hyperphosphatemia ( 6 mg/dL). Levels of phosphate in this range can aggravate of hypocalcemia. At levels above 7 mg/dL, a phosphorusbinding agent indicated. The high potassium levels lead to dysrhythmias and eventually cardiac arrest. Intravenous calcium may be ineffective as a treatment for hyperkalemia if given to a patient with hyperphosphatemia. It may be necessary to consider early dialysis. Muscles damaged by crush injury result in cell wall stretch. The stretchactivated channels in cell walls allow for inux of sodium and calcium into the cell. This results in a drop in the intravascular calcium concentration. PostreS38

perfusion, there is a calcium inux into cells. This can result in hypocalcemia ( 8 mg/dL). This is usually asymptomatic and self-correcting but can be cardiotoxic and requires replacement. The resulting hypocalcemia may also lead to cardiac dysrhythmias. Hyperphosphatemia also follows rhabdomyolysis and exacerbates the effects of the hypocalcemia.

Fluid Resuscitation in Conned Space Medicine

Fluid management in the prehospital environment is a challenging and controversial issue. The available evidence does not clearly support any single approach. Nevertheless, based on available evidence, some provisional conclusions may be drawn. The uid resuscitation and management for victims in conned spaces is aimed at the management of associated traumatic and atraumatic conditions. The cornerstone of advanced trauma life support for trauma care is the minimization of on-scene time and the rapid transport to an appropriate healthcare facility for denitive care. In the conned space environment, extended on-scene times may be unavoidable. Times may extend from less than 1 hr to several hours postincident. The traditional prehospital practice of scoop and run may not be possible. Medical complications not typically seen in the prehospital setting may be presented to the medical facility. It should not be surprising that patients may be presented to the facility in various stages of clinical deterioration. The medical complications may include: dehydration, hypothermia, environmental hyperthermia, metabolic abnormalities, airway dust impaction, untreated closed head injury, inability to practically manage any potential cervical spine injury, hypovolemia, dehydration/ starvation, and evolving cardiac arrhythmias. Patients have no nutritional intake and frequently present with an ileus and vomiting. Blood loss may recur or continue during extrication with limited hemorrhage control possibilities. Edema/ third spacing (extremities, gastrointestinal) may be quite extensive. The victim may also have experienced thermal, inhalational, or chemical burns. Field volume assessment may be based primarily on the providers index of suspicion, thirst, sensorium, vital signs (when possible), mucous membranes, and urine output. It is estimated that the amount of uid that is third spaced in extensive crush syndrome may be equal to the total extracellular volume in a 75-kg adult (2). Hypovolemic shock and acute tubular necrosis may develop if the volume of uid lost is not replaced within 6 hrs (6). The goal of uid resuscitation is to restore end organ perfusion and, therefore, oxygen delivery. Special consideration in conned space rescue is the degree of hypovolemia, extent (witnessed or
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Pulmonary Effects
Many of the pulmonary effects are secondary to the trauma associated with the entrapment event. These injuries may not be immediately evident, but the potential for these complications should be considered, especially if the patients respiratory status deteriorates. These may include rib fractures, hemothorax, pneumothorax, traumatic asphyxia, and pulmonary contusion. Pneumonia is not an immediate concern, but may present several days postextrication. It may be the result of splinting from rib fractures or as a sign of sepsis. Sepsis leading to organ failure was responsible for most of the late deaths from multiple system organ failure. The development of acute respiratory distress syndrome is one of the most serious pulmonary complications. It is believed to be triggered by release of inammatory mediators from injured cells or from direct trauma. Under these circumstances, ventilator support with positive end expiratory pressure is often needed to maintain adequate oxygenation. The event may also be complicated by fat embolism syndrome. Fat emboli form aggregates that occlude pulmonary microvasculature and cause a ventilation/perfusion mismatch. Hypoxia, hypercarbia, tachycardia, and petechia on the chest/neck are seen in association with the crush injuries and long bone fractures. The fat embolism syndrome will usually develop 23 days postinsult, and if there is presence of early hypoxia and hypercarbia, the clinician should entertain alternate sources of ventilation/ perfusion mismatch. Thromboplastin as an efux from platelet cells can trigger disseminated intravascular coagulation and subsequent respiratory failure. Aggressive uid administration in the elderly patient or those with a history of congestive heart failure may progress to pulmonary edema.

potential) of traumatic crush injury, crush syndrome also known as traumatic rhabdomyolysis, compartment syndrome, and ARF. Treatment options include the need maintain the patient as nothing by mouth if possible. This will minimize or avoid vomiting and/or aspiration. The lack or the physical inability to obtain intravenous access may dictate the need for oral hydration (least-optimal method). Any intravenous line started in the conned space setting should be considered contaminated and discontinued as soon as possible. The goal of management is early venous access only if and when it is possible. Delays in cannulation may result in signs or symptoms of hypovolemia and possibly cardiovascular instability. Medical management of crush syndrome is technically easier in the early stages of shock or rhabdomyolysis. For the entrapped patient, circulatory access should be gained on scene (in the rubble). This will not extend the overall transfer time, but will begin to treat the early stages of crush syndrome. There are multiple compelling reasons for obtaining intravenous access at the scene: uids, analgesia, and drugs for resuscitation or stabilization. Fluid options consist of the following: 1. No uid; 2. Crystalloids (isotonic and hypertonic); 3. Colloids (mainly gelatins and starch solutions); and 4. Oxygen-carrying solutions (blood and blood substitutes). Factors inuencing choice of uids are based on the early hemodynamic and clinical status. An increase in circulating volume will have a tendency to increase the cardiac output, blood pressure, and end organ perfusion. Rapid and aggressive uid resuscitation in the trauma patient may counter the protective mechanism of a lowered blood pressure and precipitate rebleeding. Uncoordinated uid resuscitation in the nontrauma medical patient may precipitate pulmonary edema. Disruption of the present state of homeostasis could result in the tendency to increase bleeding, dislodgement of primary hemostatic thrombus, vasodilation with most uids, and reduction of blood viscosity and diluting of clotting factors (with the exception of fresh frozen plasma). All these conditions could result without an increase in oxygen concentration.
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pH buffering may be necessary to counteract the acidosis from the anaerobic metabolism of energy substrate with production of lactic acid, phosphoric acid, and unoxidized amino acids. This will have negative inotropic effect and predispose the patient to arrhythmias. In the choice of uids, albumin and fresh frozen plasma have pH-buffering properties. With respect to oxygen carriage capabilities, to date, there are no articial oxygen solutions in widespread use or available for administration. Critically ill patients exhibit increased capillary permeability; albumin and water will pass into the interstitium exacerbating edema and impeding oxygen delivery. Low-molecular-weight synthetic colloids and exogenous albumin leave the circulation to a variable degree. High-molecular-weight colloids remain in the intravascular space and exert an oncotic effect, which can result in cellular dehydration. The use of some starches and hemoglobin solutions are detrimental to renal function. There have been instances of anaphylaxis with blood products and gelatins. Debate continues on the issue of crystalloid vs. colloid and the issue remains unresolved. Metaanalysis by Schierhout and Roberts at University College London Medical School 1998 demonstrated that resuscitation with colloids was associated with an increased absolute risk of mortality of 4%. Isotonic solutions are cheap, easy to store, and warm with an established safety record. They produce predictable rise in cardiac output and are generally distributed evenly throughout the extracellular space. They have the advantage to not draw water out of the intravascular space. The use of Ringers solution as the uid of choice in burns has been used for a period of time. It offers some buffering capacity, but carries the theoretical risk of iatrogenic lactic acidosis if given in large quantities in patients with liver failure. Ringers electrolyte solution contains 130 mEq/L of Na , 4 of K , 109 of Cl , and 28 of HCO3. Saline in large quantities may produce hyperchloremic acidosis. The normal saline solution is composed of 154 mEq/L of Na , 0 K , 154 of Cl , and 0 HCO3 . Hypertonic solutions are considered to have a greater ability to expand blood volume and thus blood pressure and presumptively tissue profusion, and can be administered as a small-volume load over a short period of time. Their use can

cause an osmotic shift of uid from the intracellular and interstitial spaces to the extracellular compartment. In the hypovolemic entrapped patient with a head injury, there is an increase in blood pressure without increasing the intracranial pressure (initially). The disadvantage of volume replacement may be continued bleeding from ongoing hemorrhage and exacerbate cerebral edema. In one review that compared hypertonic to isotonic crystalloids (The Cochrane review by Bunn and Roberts, February 2003), it was concluded that there is not enough data to state which one is better (further trials were needed). The consensus at present supports the use of isotonic saline as the rst-line uid in the prehospital collapse structure environment and institutional crush syndrome uid of choice. The dilemma with a hypovolemic, trauma, trapped patient is the need to balance between administering uid and, thereby, risking rebleeding and increased blood loss. The alternative option is to withhold uid and potentially allow the possibility of organ ischemia and death from hypovolemia. The concept of permissive hypotension has been advocated to allow blood pressure to remain below normal levels. The ultimate goal is to maintain vital organ perfusion without exacerbating hemorrhage (creating a rebleed situation). One method to minimize the risk of excessive uid administration is to give small boluses of 250 mL each. Different patient subgroups tolerate hypotension differently and therefore management will have to be on a caseby-case basis. For example, head injury patients require a higher pressure to maintain coronary perfusion pressure and reduce secondary brain injury, whereas patients with penetrating torso trauma probably require lower pressures. On the other hand, the elderly patient does not tolerate hypotension well. The view here is to withhold uids from trauma victims before hemorrhage control if a radial pulse can be felt. The use of 250-mL aliquots for patients with no radial pulse is a better choice than the massive historical uid resuscitations of the past. In penetrating torso trauma, the presence of a central pulse should be considered adequate perfusion. In children less than 1 yr old, the use of a brachial pulse is more practical and consistent. In the special case of the conned space crush syndrome patient, many have extensive intravascular uid decits. The
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potential for hypovolemia, arrhythmia (early), and renal failure is quite high and aggressive management is absolutely necessary. The issues and circumstances around the initiation of treatment before extrication are things that the managing physician should determine. Releasing compression coincides with the proximal early signs and symptoms of crush syndrome such as hypovolemia, shock, metabolic acidosis, arrhythmias, hyperkalemia, hypocalcemia, and hyperphosphatemia. Special considerations in conned space medicine are to rapidly reverse or stabilize hypovolemia. Intravenous access and the use of normal saline (note: Ringers lactate contains potassium), monitor for evidence of early pulmonary edema, and early renal failure. It is imperative that the potential renal injury be addressed. This requires the use of intravenous uids and alkalinization of the urine with sodium bicarbonate. The accepted crush injury cocktail during extrication is 1.5 L 0.9% NS/hr; consider adding 1 amp bicarbonate and 10 g of mannitol to each liter. Postextrication, the physician should administer 500 mL crystalloid/hr (after the initial bolus, if needed for hypotension) alternating with D5W, add 1 amp bicarbonate/L and keep urine pH above 6.5, and give mannitol if urine is 200 300 mL/hr. Consider early dialysis if oliguria develops.

is geared toward the classic description of the ve Ps: 1. Pain out of proportion to the injury/ pain on passive range of motion of the ngers or toes (patients will usually hold the injured part in a position of exion to maximally relax the fascia and reduce pain); 2. Pallor of the extremity; 3. Paralysis; 4. Paresthesias (early loss of vibratory sensation); and 5. Pulseslessness (note: when checking, an extremity pulse [dorsalis pedis] is sure to occlude the other major artery [posterior tibial artery] so that retrograde ow does not confuse the diagnosis. Compartment pressure monitoring is necessary if compartment syndrome is being entertained. Pressures measuring 30 mm Hg usually require surgical assessment. The comparison of diastolic blood pressure and compartment pressure is a relative indicator of tissue perfusion. If there is a fracture, compartment pressure measurements should be taken as close to the fracture site as possible (because these will give the highest readings) and in multiple locations. Compartment measurements within 30 mm Hg of diastolic pressure are an indication for fasciotomy (see Radical Surgical Procedures). Compartment syndrome must always be considered when the diagnosis of crush syndrome is suspected.

of 30 mm Hg (diastolic blood pressure compartment pressure). In one study, if absolute pressure were used as threshold, 52% patients would have undergone unnecessary fasciotomies. The use of differential pressure led to no missed cases of acute compartment syndrome. The present recommendation is decompression through fasciotomy if the differential pressure drops to under 30 mm Hg. Crush syndrome and muscle necrosis in a closed injury without compartment syndrome may be followed clinically until healing or demarcation of a gangrenous part occurs, providing the patients general medical condition, including renal function, can be maintained. The role of amputation is very limited in the management of crush syndrome. The early amputation of a crushed limb may not be appropriate or improve outcome, although it may expedite extrication. The eld amputation of an entrapped limb should only be a procedure of last choice. The eld amputation reects a failure of the rescue and medical system to expeditiously remove and support the victim.

Crush Syndrome in the Pediatric Patient

Children with crush syndrome who survived the 1999 Turkey earthquake were the most severely compromised patients. Their injury patterns were ankle injury (30%), thigh (28.6%), head (23.8%), and forearm (7%). It is likely that these injuries may have contributed to their incidence and complications of crush syndrome. Of this group, surgical amputations and multiple fasciotomies were performed on 12.6% of this pediatric population. Acute renal insufciency occurred in 27% of the children.

Compartment Syndrome in Crush Syndrome

Compartment syndrome is the elevation of interstitial pressure in closed fascial compartment that results in microvascular compromise, myoneural dysfunction, and secondary tissue hypoxia. Increased pressure within this conned space leads to microvascular compromise and subsequent cellular death. Systemic hypotension, limb trauma, interstitial tissue pressure of 30 mm of mercury has been suggested as threshold at which there is the diagnosis of compartment syndrome. The associated pathophysiology is compressive damage to these muscle groups, which results in local swelling and bleeding. As a result of the inelasticity of the fascial compartment, swelling occurs inward, resulting in compressive forces and collapse of blood vessels, nerves, and muscle cells. If hypoxia continues, the cells will undergo necrosis. The compartment syndrome examination
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Radical Surgical Procedures

There are many advocates for the early use of denitive surgical intervention. Some feel that crush syndrome with prolonged muscle compression and associated compartment syndrome require some level of operative management. Medical management of systemic complications, along with operative procedures of fasciotomy and debridement, are indicated with accompanying severe compartment syndrome. There are those who maintain the position that the combination of delayed rescue, delayed fasciotomy, and delayed radical debridement may worsen the long-term prognosis. The current consensus is that the use of fasciotomy for the management of crush syndrome is not associated with an improved outcome when considering the patient fasciotomy by comparing the threshold of 30 mm Hg as an absolute pressure vs. using a differential pressure

Pathophysiology
Like in the adult, injury to tissue causes cell damage release of potassium, myoglobin, and phosphate into circulation. The inux of sodium and uid into cells can lead to hypovolemic shock, hyperkalemia, metabolic acidosis, compartment syndrome, and ARF. There is limited information on the affects of crush syndrome on the pediatric patient. The Marmara, Turkey, earthquake in 1999 had a signicant number of pediatric victims. Studies from this earthquake demonstrated the fact that children are not little adults! They have
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different physiological responses to stress, have less elastic tissue, are smaller, with a more compact body mass, and a have an increased ratio of surface area to body volume. Their smaller body mass often results in a greater distribution of injuries. Therefore, multisystem injuries should be considered the rule rather than the exception. A childs response may be only to increase heart rate to maintain cardiac output, whereas respiratory failure is usually the precursor to cardiac failure. This should be monitored and reassessed on a frequent basis. Physiological compensation appears capable until the point of sudden collapse. Abnormal tachycardia may be the only hint of hypovolemia. Children are often difcult to assess and may not be able to communicate events or injuries. Additionally, they have an increased risk of heat and insensible uid loss. Smaller spaces with less elasticity may place child at increased risk for compartment syndrome. Management is not unlike the adult with the basis of management being the aggressive intravenous hydration with normal saline at a rate of 10 20 mL/kg per hour. Special attention to heart rate, alkalinization, and serum peak creatine kinase levels as important indicators of potential renal dysfunction. In Marmara, Turkey, at 1:37 am, on August 17, 1999, A 7.4 Richter scale earthquake struck the Northwest region of Turkey. This area had a population of approximately 16 million people. The earthquake resulted in 15,000 deaths, 40,000 serious injuries, and destroyed approximately 75,000 buildings. In this incident, nearly 90 children were diagnosed with crush syndrome (as reported by the Registry of Turkish Nephrology Association). From this event, most of the current pediatric crush management infor-

mation was derived. Donmez (7) reviewed the impact on children at the Marmara earthquake. The study looked at 40 children 15 yrs old. From this group, ve children were found to be in severe shock from trauma died, four were referred to other centers for care, 11 were treated as outpatients, and 20 were diagnosed with crush syndrome. This group consisted of seven boys and 13 girls, with a mean age of 10.2 yrs (3.5 mos to 15 yrs). Their extrication time varied from 3 to 98 hrs (mean, 18 hrs). Intravenous uids were started at the rescue area (and continued to the medical treatment area) in eight children. None of these patients developed ARF. All of these patients received 2,500 3,000 mL/m2 diuretics, alkaline treatment, antibiotics if infection was diagnosed, and a few received albumin. The laboratory tests showed a mean peak creatine kinase of 18,099 (range, 280 86,460); K ranged from 3.2 to 8.2. Injuries found were 11 with one extremity injury, nine with 1 injury, and 15 required fasciotomy; of these, two had amputations of one extremity and two had bilateral amputations. Acute renal failure occurred in seven children (35% of all 20), but no intravenous uids were started before admission in seven of 12 (58%). Of this group, four of these seven needed hemodialysis. All returned to normal renal function. Six of these seven had multiple extremity injuries. One died of sepsis during hemodialysis. Iskit and colleagues (8) studied 33 patients 16 yrs old (16 girls and 17 boys; aged 14 days to 16 yrs). Of this group, 15 were diagnosed with crush injury, 10 had acute renal failure, and two required hemodialysis. Six children required fasciotomy for compartment syndrome (no amputations).

It is evident from these studies that crush syndrome is not solely an adult disease. Aggressive and early management of children can signicantly impact on their morbidity and mortality.

CONCLUSION
The management of crush syndrome requires the clinician to maintain a highindex of suspicion. The on-scene treatment may be limited by the circumstances of the rescue, and therefore initial care may ultimately prove to be inadequate. Overall aggressive treatment is necessary to decrease mortality and morbidity from the time of contact in the eld and from the emergency department to the intensive-care setting. The treatment in the acute phase of the rhabdomyolysis consists of maintaining adequate circulating volume and sufcient diuresis to prevent renal, cardiac, and pulmonary complications.

REFERENCES
1. Pepe E, Mosesso VN Jr, Falk JL: Prehospital uid resuscitation of the patient with major trauma. Prehosp Emerg Care 2002; 6:81 91 2. Better OS: Management of shock and acute renal failure in casualties suffering from the crush syndrome. Ren Fail 1997; 19:647 653 3. Bywaters EGL: Ischemic muscle necrosis. JAMA 1944; 124:1103 4. Bywaters EGL, Beall D: Crush injuries with impairment of renal function. BMJ 1941; 1:427 432 5. Zager RA: Lab Invest 1989; 60:619 629 6. McQueen, et al: Compartment monitoring in tibial fractures: The pressure threshold for decompression. J Bone Joint Surg [Br] 1996; 78:99 104 7. Donmez, Osman, et al: Crush syndrome of children in the Marmara Earthquake, Turkey. Pediatr Int 2001; 43:678 682 8. Iskit, et al: J Pediatr Surg 2001; 36:368 372

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