BY TONY GARCIA
The recent 7.0-magnitude earthquake in Haiti trapped thousands under the rubble of collapsed buildings. News media reported dramatic rescues and raised questions about those who remained buried awaiting rescue. Victims who were located and freed face a long and difficult path to recovery because of the complications that often arise after a crush injury.
The crush injury syndrome was first recognized and described during World War II in trapped victims rescued from collapsed buildings during the bombing of London, England. It was identified in victims who had one or more extremities trapped under debris for extended periods.1-6 In the current literature, building collapses resulting from earthquakes have the highest incidence of crush syndrome (Table 1). (1) Crush syndrome is also seen in victims of mine collapses, industrial accidents, and explosions. (5) It has also been reported in situations where a patient with altered mental state (e.g., as a result of a stroke or an overdose) crushes a part of his body with his own weight or after suffering a severe, brief pressure across a limb (such as from an automobile). (4, 5)
The terms crush injury, crush syndrome, compartment syndrome, and traumatic rhabdomyolysis are often used interchangeably. To reduce confusion, a consensus panel in the United Kingdom has simply defined a crush injury as a direct injury resulting from crush and crush syndrome as the systemic manifestation of muscle cell damage resulting from pressure or crushing. (2, 3) Compartment syndrome, a condition in which the pressure within the muscle compartment rises to critically high levels resulting in severe ischemia, is closely associated with crush injury or syndrome and can occur simultaneously or independently. Crush syndrome is frequently observed because of prolonged (>4 hours) entrapment, although cases resulting from brief (<1 hour) entrapment have also been reported. (5) The duration of ischemia will determine the degree of muscle injury the patient experiences.
When compressive forces damage muscle tissue, the cell membrane stretches and leaks, spilling its contents into the extracellular space; this is called rhabdomyolysis. Among the contents are the muscle protein, myoglobin, and potassium (K+), the chief intracellular cation. Additionally, because of the increased permeability of the cell membranes, calcium (Ca++), an extracellular cation, migrates into the damaged cells. During extended periods of entrapment, perfusion to the injured extremity is reduced and those tissues suffer from prolonged ischemia (two to four hours of ischemia lead to irreversible changes and ischemia >6 hours leads to muscle necrosis). (5) This results in the development of an anaerobic metabolism within the already damaged tissue, adding insult to injury. As entrapment time increases, the pressure within the extremity continues to build, and the injured tissue will continue to leak cellular contents and produce lactic acid until the extreme weight is removed. It is at this point that most patients, under these conditions, begin to suffer the consequences of crush syndrome. (1, 2, 4, 5)
When the source of pressure from the crushing injury is removed, the cellular debris and waste products stagnating within the injured extremity are no longer confined to the injury area and are free to circulate. The sudden return of these constituents to the central circulation, coupled with the potential space that exists within the injured muscle mass, lead to a series of events known as reperfusion syndrome; these begin to define the systemic consequences of crush syndrome. (1, 2, 4, 5)
Metabolic derangements. Remember that when the cells were damaged from the crush, the injured cells released potassium into the extracellular space and anaerobic metabolism led to the production of lactic acid. The heart is very sensitive to even slight derangements in potassium balance as well as shifts in the acid-base balance within the body. A sudden influx of potassium or lactic acidosis can result in immediate life-threatening dysrhythmias. This is the most common reason a crush injury patient will deteriorate rapidly into cardiac arrest after the pressure is released.
Acute renal failure(ARF). The large quantity of myoglobin that was released during the crush is now free to circulate. Myoglobin is a relatively large protein that can readily combine with other proteins that are also circulating in the blood. When the myoglobin does combine with other blood proteins, such as albumin, it forms casts in the bloodstream. These are too large for the kidneys to filter, and they become clogged and unable to function, resulting in ARF. Brown- to rust-colored urine is an early indicator that the kidneys are processing an excessive amount of myoglobin. ARF is frequently seen several days post-injury and can be eliminated altogether if treatment is initiated early. (1, 2, 4, 5)
Hypovolemia.The crushed muscle tissue has the capability of sequestering large volumes (up to 12 liters in a 75-kilogram adult) of blood and other fluids in the immediate period (more than 48 hours) after the crush injury. (4, 5) Because of the sequestration (third-spacing), the patient can develop hypotension from the ensuing hypovolemia. As fluids are confined within the injured extremity, the pressure within the affected limb will continue to rise, potentially leading to compartment syndrome. Additionally, the kidneys are extremely sensitive to decreases in perfusion (they are perfusion “hogs,” requiring 25 percent of cardiac output), adding additional insult to an already taxed pair of organs and exacerbating ARF. (4, 5) Hypovolemia, secondary to third-spacing, is the primary cause of death in the intermediate (four days) period after crush injury and is often the first manifestation of crush syndrome.
Prehospital management. Basic life support includes c-spine precautions if the incident circumstances so dictated, the administration of oxygen, and appropriate management of long bone and soft tissue trauma. Local protocol will dictate advanced care but should include, at a minimum, ECG monitoring and management of potential dysrhythmias from electrolyte abnormalities and aggressive fluid resuscitation.
You must take extreme care to prepare the patient for removal to attempt to minimize the damaging effects on the kidneys. Treatment of earthquake victims has demonstrated that initiation of fluid resuscitation within the first six hours improves outcome in crush syndrome. The preferred fluid in the prehospital setting is 0.9 percent normal saline. Avoid using Ringer’s lactate solution—it contains potassium, and the patient is likely to already be hyperkalemic from the crush injury’s metabolic effects. (1-6),7 You should initiate fluid resuscitation while the victim is still trapped to effect hydration to prevent hypotension and forced diuresis to prevent ARF. (1-7) Until urine output can be measured to assess the effects of hydration, administer normal saline at a rate of 1.5 liters per hour. Once urine output can be measured, fluid administration should be titrated to maintain a urine output >300 ml/hr. (1,2,4,5) Once the victim has been released, the 0.9-percent normal saline IV fluid should be alternated with 0.45 percent normal saline/D5W IV fluid to minimize the sodium load on the patient; the rate of infusion should remain the same.(4, 5)
The patient should also receive sodium bicarbonate with every other bag of IV fluids. This is accomplished by adding 50 mEq of 8.4-percent sodium bicarbonate to the IV bag and infusing at the previously mentioned rate. (1-7) Administering sodium bicarbonate counteracts the acidosis associated with anaerobic metabolism and increases (alkalinizes) the urinary pH. Alkalinization of the urine increases the solubility of myoglobin, preventing the formation of the renal casts and promoting the myoglobin excretion. Once the urine pH can be measured, keep it above 6.5 by administering sodium bicarbonate.
Although most EMS systems do not routinely carry mannitol, it may prove beneficial to the crush syndrome patient during an extended extrication. Some of the reports from previous earthquakes suggest that mannitol increases diuresis and behaves as a scavenger of oxygen-free radicals that can pose additional harm to the already delicate kidneys. (4-7) Administer 1-2 g/kg of a 20-percent mannitol solution over the first four hours. More recently, mannitol’s effectiveness in preventing renal insult has been increasingly questioned.
Additional considerations. If the patient develops hyperkalemia, as evidenced by tall, peaked T-waves, disappearing P-waves, and intraventricular conduction defects (QRS widening), administering intravenous calcium chloride or the combination of insulin and glucose might be helpful. (4-7) Calcium chloride directly antagonizes the effects of potassium, which helps to “stabilize” the myocardial membrane. Administering insulin and glucose promotes the movement of potassium back inside the cells, thereby helping to correct the hyperkalemia. Additionally, if you are performing a critical care transfer of a crush injury patient, the patient may benefit from the administration of polystyrene sulfonate (Kayexalate) prior to transfer. (4-7) Kayexalate is an exchange resin that binds potassium within the gastrointestinal tract.
Hemodialysis.Closely monitor patients with significant injury for evidence of ARF. One indicator of hemodialysis is decreased urine output (oliguria) despite increased hydration. (1, 4, 5) Additionally, intractable hyperkalemia and acidosis that is nonresponsive to sodium bicarbonate administration is another indicator for hemodialysis. This was first observed in the aftermath of the 1988 Armenian earthquake in which at least 225 victims required dialysis as a result of injuries sustained from this event. (1) The lack of a coordinated response to this need resulted in chaos, which created a secondary disaster. Recognizing the need to provide a coordinated response in future disasters, the International Society of Nephrology established the Renal Disaster Relief Task Force. (1, 4) This team of specialists will respond to provide increased capacity to perform hemodialysis to mass casualties at an earthquake. Since its inception, the team has responded to every major earthquake and has proved invaluable.
Although crush syndrome is relatively rare, recent events are a sobering reminder that EMS personnel must be ready to manage patients who suffer this damage. Early recognition that the potential exists for crush syndrome to develop will be the all-important first step. Aggressive management to correct the syndrome’s negative consequences will reduce morbidity and mortality from this rare condition.
1. Sever MS, R Vanholder, N Lameire, “Management of Crush-Related Injuries after Disasters.” N Engl J Med.; 2006, 354(10):1052-63.
2. Smith J, I Greaves, “Crush Injury andCrush Syndrome: A Review.” JTrauma; 2003, 54(5)(suppl):S226-S230.
3. Greaves I, K Porter. “Consensus statement on crush injury and crush syndrome.” Accident and Emergency Nursing; 2004,12(1):47-52.
4. Gonzalez D, “Crush Syndrome,” Crit Care Med.; 2005, 33(1)(suppl):S34-S41.
5. Malinoski D, M Slater, R Mullins, “Crush Injury and rhabdomyolysis,” Crit Care Clinics; 2004, 20(1):171-192.
6. Sahjian M, M Frakes, “Crush Injuries: Pathophysiology and Current Treatment,” The Nurse Practitioner; 2007, 32(9):13-18.
7 . Centers for Disease Control and Prevention. Blast Injuries: Crush Injuries and Crush Syndrome.Available at: www.bt.cdc.gov/masscasualties/.blastinjury-crush.asp. Accessed March 18, 2009.
TONY GARCIA, RN, CCEMT-P, is a training specialist with the TEEX Emergency Services Training Institute in College Station, Texas. He has more than 25 years of public safety experience in fire, EMS, and law enforcement. Garcia serves within the incident management training programs grant-funded by the Department of Homeland Security (DHS), providing training and technical assistance throughout the United States.