On January 17, 1994, the Northridge Earthquake struck Los Angeles, California. Inside a three-story reinforced concrete parking garage, Salvador Peña was operating his street sweeper. As the quake struck, the structure collapsed on top of Peña, trapping him in the sweeper under concrete support beams. For nine hours, members of the Los Angeles City and County Fire Departments worked to free Peña, dealing with operational issues including working in an unstable structure, the possibility of aftershocks, spilled fuel from the sweeper, and the possibility of Peña’s initial injuries progressing to crush syndrome during the rescue.
As paramedics gained access to the patient, they evaluated and cared for Peña’s crush injuries and treated him for crush syndrome as the concrete beams were lifted. Throughout the operation, paramedics coordinated care with UCLA Medical Center, where Peña was ultimately flown for additional treatment. Without careful coordination among the urban search and rescue team, emergency medical services (EMS), and the destination hospital, Peña’s condition might have had a very different outcome.1
Crush Injury
Physical entrapment can be associated with a variety of problems including soft tissue, inhalation, blast, and musculoskeletal injuries; thoracoabdominal trauma; and burns. A crush injury is defined as compression of muscle mass causing damage, compromised circulation, and swelling.2 The most commonly affected areas are the lower limbs (74 percent), the upper extremities (10 percent), and the trunk (nine percent). (2)
On the positive side, compression of the trapped body parts may provide a temporary tamponade effect, staunching internal and external bleeding in the compressed area while the pressure remains in place.3 As long as the patient remains trapped, the “squeezing” of the crush injury increases relative blood volume in the rest of the body as blood is pushed out of the trapped area. (3) For example, a patient trapped up to his waist in debris will likely have some of the blood in his legs temporarily squeezed up into his chest and upper body.
On the negative side, as the body is compressed, direct damage occurs to cells, causing swelling and allowing cell contents to leak out.4,5 As swelling continues, it increases pressure on the compressed area, further reducing blood flow to that area. (4, 5) The swelling can be so severe that circulation may not resume even after the pressure has been released; this is known as compartment syndrome.6 As blood flow is reduced (hypoperfusion), tissues become deprived of oxygen and nutrients; wastes build up; and the cells begin to break down, allowing even more cell contents to leak out. (4, 5)7-12
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| (1) With crush injuries, perfect coordination between the rescue crew and EMS is more important than speed of extrication (Photos by author.) |
The “skin” of muscle fibers (sarcolemma) is responsible for moving sodium, potassium, and other electrolytes in and out of cells. A normal, resting muscle fiber (muscle cell) has potassium phosphate on the inside and sodium chloride on the outside. (4) Within the muscle cells are numerous enzymes, proteins, and other materials. (4) These chemicals – crucial to muscle function – are harmless as long as they are contained within the walls of the sarcolemma. When cell walls break down, either because of trauma or tissue ischemia, these chemicals leak out and wreak havoc on the body; this leakage is known as rhabdomyolysis. (4) When rhabdomyolysis occurs from impact or compression trauma, it is referred to as “crush” injury. Rhabdomyolysis (muscle breakdown) can also be caused by extreme muscle exertion, ingestion of certain drugs, or even just lying on a hard surface for a prolonged period of time (such as an elderly person who falls while home alone). (4)13 Although rhabdomyolysis can begin in as little as one hour, signs and symptoms will present within four to six hours of compression. (3)
As rhabdomyolysis occurs, cells leak out their toxic cellular contents and absorb sodium, water, and calcium, resulting in insufficient calcium remaining in the body for normal muscle and heart function. (4) As long as a part of the body remains under compression, the lack of circulation also means that these toxins cannot yet affect the rest of the body. (4) Although these leaked materials cannot be seen directly, clues to their presence can be found using the five “Ps” of crush injury: pain, pallor (pale color), paresthesias, paralysis, and pulselessness.14 If any part of a patient has been under pressure against a hard surface for four to six hours or if you find any of these five Ps, you can presume that rhabdomyolysis has begun and is likely to lead to crush syndrome when compression is released and blood flow is restored to the damaged area. (3)
Crush Syndrome
Although crush injury and rhabdomyolysis are basically hypoperfusion (low blood flow) injuries, crush syndrome is a reperfusion (return of blood flow) injury.
The first detailed cases of crush syndrome were observed in 1941, as victims of the bombing of London were pulled from collapsed buildings. Many survived their initial injuries but later died or developed swollen limbs, dark urine, and kidney failure. (4) This syndrome was originally named Bywaters’ Syndrome after the doctor who discovered it. (4)
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| (2) An inside medical provider should be properly equipped and trained to make contact with the victim and protect, assess, treat, and prepare him for extraction. |
Crush syndrome is comprised of three major mechanical issues and three major chemical problems, which follow (three mechanical problems occur once the pressure is released, freeing the victim):
- Swelling may continue, leading to compartment syndrome (tissue ischemia because of pressure from the inside out).
- Bleeding will resume where pressure is released.
- Blood pressure will drop as blood flow returns to the now freed area.
In addition, when the trapped body area is released and blood flow is restored, built-up wastes and damaged cell contents are released. Although they include a wide variety of toxins, three major chemical problems can occur:
- Acidosis. Produced by ischemia, acidosis inhibits normal cellular activity and can cause systemic vasodilation, further dropping blood pressure and plunging the patient into shock.
- Myoglobin. Generally nontoxic in blood of normal pH, myoglobin breaks down into ferrihemate in acidotic blood. Ferrihemate clogs up the kidneys, resulting in kidney failure, disturbing fluid balance and the ability to remove toxins in the blood.
- Potassium. Directly affects the flow of electricity in the heart, leading to problematic, if not fatal, dysrhythmias. It is detectable on an electrocardiogram (ECG), first as tall peaked T waves progressing to absent P waves and widened QRS complex and gradually progressing to ventricular tachycardia and ventricular fibrillation.
As trapped limbs are freed, a sudden increase in preload occurs as cold, toxin-filled blood rushes back to the heart while, at the same time, afterload suddenly drops as blood from the heart flows back into the limbs and bleeding increases. The aim of treatment is to make this inevitable process as slow and as controlled as possible. Remarkably, the area crushed and the duration of entrapment do not appear to have a significant effect on the severity of crush syndrome.
Operations
Rescuers should be familiar with situations likely to require technical rescue and crush injury/syndrome care. These situations include prolonged motor vehicle extrication, trench collapse, silo entrapment, earthquakes, tornadoes, mud/rock slides, industrial accidents, and structural collapses.15
Successful rescue operations demand a robust command system and clear communications. This is especially important during operations where the victim is entrapped for a prolonged period of time. Assessment and direct patient care begin at size-up; continue through gaining access, disentanglement, packaging, removal, and transport; and end with a coordinated patient hand-off at the destination trauma or specialty care center.
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| (3) Fire, rescue, and emergency medical services must train together to be able to effectively coordinate the rescue victims of crush injury. If they fail to do so, a “successful” rescue may be turned into a fatality by the resulting crush syndrome. |
The inside medical provider (IMP, or whatever local term is used) will contact the victim; protect, assess, and treat as necessary; and facilitate removal. Keep in mind that only properly trained and equipped personnel should attempt to gain access to hazardous and technical environments. It is crucial that you coordinate among rescuers; the IMP; and advanced medical resources, including the destination hospital.
If the potential for crush syndrome exists, rapid removal may not be the best option for the patient. For example, one victim of the 1987 Amtrak collision in Silver Spring, Maryland, was trapped in the wreckage for 12 hours. She remained conscious, alert, and oriented throughout her ordeal; but, within 15 minutes of extrication, she went into cardiac arrest and died despite advanced life support care and rapid transport to a local trauma center.
Assessment and Treatment
Crush injuries and associated trauma should receive standard trauma treatment but with the recognition and preparation to treat crush syndrome. You can divide crush syndrome-specific treatment into the following steps taken before extrication, immediately prior to release, and after extrication.
Before Extrication
- Airway/breathing. Keep in mind that the victim will still need the same – if not greater – respiratory protection as rescuers. Even for patients who can maintain their own airway, consider dust masks, supplemental oxygen, and other adjuncts as appropriate for their environment. If advanced airway adjuncts such as endotracheal intubation and placement of a supraglottic airway are necessary prior to extrication, consider the use of a portable ventilator to facilitate extrication.
- Circulation. Identify and stop heavy external bleeding using standard tools and techniques such as direct pressure, tourniquets, hemostatic gauze, and pressure bandages. Assess and anticipate significant internal bleeding that might begin once the entrapped body part is released. Keep in mind the possibility of patient dehydration because of prolonged entrapment of hours to days. Gain intravenous or intraosseous infusion access and consider 20 ml/kg of 0.9 percent saline administration for volume replacement as well as to preserve kidney function. Avoid Lactated Ringer’s solution; it will contribute further to hyperkalemia. Consider using a pressure infuser if patient access does not allow effective gravity feed of solution.
- Drug administration. Consider administration of pain control medications such as morphine, fentanyl, or ketamine along with antiemetic medications such as ondansetron. Likewise, consider administration of anxiolytics such as midazolam, diazepam, or lorazepam.
- ECG monitoring. Establish continuous cardiac monitoring and treat dysrhythmias accordingly.
Immediately Prior to Release
- Airway/breathing. Keep in mind that the victim will likely need the same, if not greater, respiratory protection as rescuers because rescue efforts may worsen a hazardous atmosphere. Even for patients who can maintain their own airway, consider dust masks, supplemental oxygen, and other adjuncts as appropriate for their environment.
- Circulation. The application of tourniquets to slow the progression of crush syndrome remains controversial, with only one or two case reports suggesting benefit. If applied for this purpose, place tourniquets just prior to extrication and have them remain in place throughout transport. Continue administration of 0.9 percent saline at 5mL/kg/hr.
- Drug administration. Consider administering sodium bicarbonate 2 mEq/kg IV/IO to treat expected acidosis and hyperkalemia.
- ECG monitoring. Anticipate cardiac dysrhythmias beginning or significantly worsening as the patient is extricated. Watch for signs of hyperkalemia including tall, peaked T waves; flattened or absent P waves; and widened QRS complexes.
After Extrication
- Airway/breathing. Anticipate the need for advanced airway and breathing management because of the onset of acute respiratory distress syndrome (ARDS) once the patient is extricated.
- Circulation. Continue administration of 0.9 percent saline.
- Drug administration. If hyperkalemia is suspected, consider administering 10-percent calcium chloride (10 mL in a line separate from the one used for administration of sodium bicarbonate). Also, consider administering nebulized albuterol to stimulate intracellular uptake of excess potassium as well as reverse histamine induced bronchoconstriction.
- ECG monitoring. Continue to monitor for tachydysrythmias including ventricular arrhythmias and signs of hyperkalemia.
In the event of any prolonged period of pressure on a limb or body part against a hard surface, whether the patient is the victim pinned under a structural collapse or lying on the floor because of a stroke, consider the externally visible signs of crush injury and the hidden threat of crush syndrome.
How much of the body is trapped and for how long matter much less than how early treatment for crush syndrome is prepared and how well advanced care is coordinated with rescue efforts. Visible crush injuries may be painful and debilitating, but the “silent crush syndrome” that follows can be deadly if it is not prevented by coordinated efforts of rescuers and EMS providers.
References
1. Ibers W, Devarney K, Siedel G, and Collins L. Search and Rescue Operations Following the Northridge Earthquake. United States Fire Administration (usfa.fema.gov, 1996).
2. “Crush Injury and Crush Syndrome.” American College of Emergency Physicians – Crush Injury and Crush Syndrome. acep.org (2009). Available at: https://www.acep.org/MobileArticle.aspx?id=46079&parentid=740 (Accessed December 8, 2016).
3. Anesthesia Trauma & Critical Care. Anesthesia Trauma & Critical Care Course Manual (atacc.co.uk, 2014).
4. Greaves I, Porter K, and Smith J. Consensus statement on crush injury and crush syndrome. Trauma 4, 129-134 (2002).
5. Smith J. and Greaves I. Crush Injury and Crush Syndrome: A Review. Journal of Trauma and Acute Care Surgery 54, S226 (2003).
6. “Compartment Syndrome.” Compartment Syndrome – National Library of Medicine, PubMed Health. PubMed Available at: https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024266 (Accessed December 9, 2016).
7. Demirkiran O, Dikmen Y, Utku T, and Urkmez S. Crush syndrome patients after the Marmara earthquake. Emergency Medicine Journal 20, 247-250 (2003).
8. Sever MS. The Crush Syndrome (and Lessons Learned from the Marmara Earthquake). S Karger Ag (2005).
9. Yokota J. Crush Syndrome in Disaster. Japan Medical Association Journal 48, 341-352 (2005).
10. Gonzalez D. Crush syndrome. Critical Care Medicine 33, S34-S41 (2005).
11. Sahjian M and Frakes M. Crush injuries: pathophysiology and current treatment. Nurse Pract 32, 13-18 (2007).
12. Sever MS and Vanholder R. Management of crush victims in mass disasters: highlights from recently published recommendations. Clin J Am Soc Nephrol 8, 328-335 (2013).
13. Genthon A and Wilcox SR. Crush syndrome: a case report and review of the literature. J Emerg Med 46, 313-319 (2014).
14. Piepenburg C. Prehospital Management of Crush Injuries. fireengineering.com (2006).
15. Burns K, Cone DC, and Portereiko JV. Complex extrication and crush injury. Prehosp Emerg Care 14, 240-244 (2010).
ROMMIE L. DUCKWORTH is a career fire captain and paramedic emergency medical services coordinator for the Ridgefield (CT) Fire Department. He has more than 25 years of experience working in career and volunteer fire agencies, public and private emergency services, and hospital-based health care systems. He is a frequent speaker at national conferences and a regular contributor to research programs, magazines, and textbooks on fire and emergency service topics.
Other Toxic Cellular Materials Released into the Body After Crush Injury
- Adenosine: produces heart block.
- Phosphorus: aggravates hypocalcemia, toxic to kidneys.
- Lactic acid: vasodilation, contributes to myoglobin conversion to ferrihemate.
- Uric acid: toxic to kidneys in high concentrations.
- Thromboplastin: contributes to disseminated intravascular coagulation or uncontrolled blood clotting throughout the body.
- Histamine: constriction of smooth muscle in lungs and vasodilation.
- Nitric oxide: can cause systemic vasodilation and renal vasoconstriction.
- Inflammatory and immune system mediators: triggers systemic inflammatory response syndrome and possible acute respiratory distress syndrome.
- Tyrosine: converted to L-DOPA; then to dopamine and norepinephrine; and finally to epinephrine, which can contribute to tachydysrhythmias.
Rommie L. Duckworth will present “Crush Injury, Crush Syndome, and Compartment Syndome in Technical Rescues” at FDIC International in Indianapolis on April 27, 2017, 3:30 p.m.-5:15 p.m.
PREHOSPITAL MANAGEMENT OF CRUSH INJURIES
Recognizing and Treating Crush Syndrome
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