Beyond the Basics: Crush Injuries and Compartment Syndrome

You respond to the scene of a car versus semi truck. The truck driver is ambulatory without complaints and is being managed by the first responders. As you approach the car, you find the driver trapped under the dashboard and complaining of severe pain to his lower extremities; however, you cannot gain adequate access to his legs. Several hours later, extrication efforts have failed because of the way the victim is trapped within the vehicle. This patient has a great potential for suffering a crush injury or developing a compartment syndrome. In addition to ensuring that the patient has a patent airway, adequate breathing and perfusion, what other concerns do you have for him? What specific emergency care would you provide? Read on for the answers to these and other questions.

Pathophysiology

Crush injury (CI) and compartment syndrome (CS) are different processes with similar pathophysiology that are frequently discussed synonymously. A crush injury results from prolonged continuous pressure on large muscles like those of the legs or arms, which results in muscle disintegration. Compartment syndrome can be defined as any condition in which a structure such as a nerve or tendon has been constricted within a space. Compartment syndrome is most often associated with deep tissue injury that results in a restriction of outward swelling caused by a collection of blood in the injured tissue due to the inflexible muscle fasciae. This results in increased pressure within the space and swelling that is concentrated inward toward the injured and uninjured tissues and structures. Compression of the internal structures forces restriction of blood flow because capillaries are compressed by the high compartmental pressures.

Venous pressure increases and the arterioles spasm, leading to tissue ischemia, swelling and, potentially, tissue necrosis. Think of the pericardial tamponade patient: When the pericardial sac is filled and stretched to the point where it will stretch no more, pressure begins to shift away from the sac and toward the heart until it can no longer fill and contract effectively. This same principle of pressure applies in a crush injury. The skin will only stretch so far. As pressure builds within an extremity, it is eventually transmitted inwardly from the skin to the vessels and other internal structures.

Although trauma is the most likely cause of CS/CI, it can also occur in non-traumatic situations. An extremity that is compressed for a long period of time beneath the weight of the patient's own body, such as after suffering a stroke, is prone to compartment syndrome. Another cause may be muscle overexertion to the point where rhabdomyolysis develops.

The most prominent type of body muscle is skeletal muscle. Skeletal muscle cell membrane, also known as sarcolemma, is a key factor in ensuring normal cell function and in maintaining a normal cell structure. The cell membrane contains pumps that move potassium and calcium to the inside of cells and sodium to the outside. These pumps rely on energy in the form of adenosine triphosphate (ATP). Myoglobin, a protein found within the skeletal muscle cell, is responsible for supplying skeletal and cardiac muscles with oxygen. The myoglobin has a greater affinity for oxygen than hemoglobin; thus, oxygen is drawn into the skeletal muscle cells from the blood to be used in normal cell metabolism. The skeletal cell also contains enzymes that are not harmful to the cell itself unless the intracellular calcium level rises. When the calcium level rises, the enzymes become destructive to the cell structure and cause its membrane to leak or rupture.

Damage to the skeletal cell membrane, from either direct injury or loss of ion pump, allows calcium and sodium to rush inside the cell, resulting in leakage of myoglobin, potassium, uric acid and phosphorus. These substances collect in the interstitial fluid (fluid around the cell) and may eventually be picked up by the capillary network and circulated in the blood, leading to more systemic complications. This process is referred to as rhabdomyolysis.

Potassium is an electrolyte that has profound effects on the heart, leading to cardiac rhythm disturbances that may be lethal. Myoglobin, which stores oxygen for times of exertion and is normally found in muscle tissue, is released into the patient's circulation due to the sustained pressure of compartment syndrome. The kidneys are unable to filter the large myoglobin molecule, which can totally obstruct renal blood flow and lead to kidney failure and death.

Amino acids and other organic acids are released as the result of tissue and muscle death. These molecules contribute to acidosis, aciduria and dysrhythmias. Tyrosine, an essential amino acid, is first converted to L-DOPA, then to dopamine and norepinephrine, and finally to epinephrine, which can contribute to development of tachydysrhythmias.

Formed when oxygen is reintroduced into ischemic tissue, oxygen free radicals, superoxides (O₂-) and peroxides (O₂₂-) are oxygen molecules that contain an unpaired electron in their outer shell. As a result, the molecules become highly chemically reactive. As with all stable molecules, the outer layer of the electron shell must be filled and the free radical must pull a second electron from a neighboring molecule. This begins the cascade of free radical propagation. The major source of free radicals is leakage from the electron transport chains of the mitochondria, chloroplasts and endoplasmic reticulum.

Table 1 lists other chemicals, enzymes and compounds released during the CS/CI event.

In a healthy patient, blood leaves the extremities via the venous vessel, removing carbon dioxide and waste products from the tissues. In either CS or CI, compression of the extremity impedes venous blood flow. Although venous flow is obstructed, the higher arterial pressure allows for continual arterial blood flow, creating significant pressure within the injured tissue with no outlet for the arterial flow.

The lack of effective perfusion resulting from one of these injuries begins a cascade toward serious illness or death. Inadequate blood flow through the extremity leads to tissue ischemia followed quickly by metabolic acidosis. If the compression is unrelieved and poor perfusion is not corrected, the affected tissue will eventually begin to die.

Once the obstruction of blood flow is corrected, the toxic substrates that have been forming within the tissues of the compressed or crushed extremity are released into the patient's systemic circulation, potentially resulting in metabolic acidosis. A side effect of metabolic acidosis is widespread vasodilation, which may produce a relative hypovolemia from maldistribution of blood volume. Metabolic acidosis and high potassium levels could have deleterious effects on the myocardium and lead to patient death.

Ventricular fibrillation is the most common dysrhythmia associated with sudden cardiac death in the CS/CI patient. It is important to note that because of the elevated phosphate levels and subsequent decrease in calcium, the potassium is left unopposed and can directly impact the myocardial cells. Calcium has been shown to be cardio-protective and, in the case of a CS/CI, the lack of calcium can expose the myocardium to significant risk for the untoward effects of high potassium levels. Serum potassium levels between 7–8 mEq/l often contribute to development of ventricular dysrhythmias. If uncorrected, and potassium levels reach the range of 8–10 mEq/l, the QRS complex continues to widen and eventually blends with the T wave, producing the classic sine-wave electrocardiogram. Once this occurs, ventricular fibrillation and asystole are imminent.

As potassium is being liberated into the systemic circulation, myoglobin is diffusing into tissue through dilated vessels. Normally, a release of myoglobin into the tissue is not detrimental, because it is soluble in blood in the presence of a normal pH. However, in the case of a CS/CI, the blood pH will likely be decreased due to metabolic acidosis, thus causing a rapid flow of blood and large myoglobin molecules into the tissue and often leading to renal failure.

Recognizing a crush injury or compartment syndrome is highly dependent on obtaining an accurate clinical history and, to some degree, the physical examination. A history of a crush injury mechanism or a suspected period of limb ischemia with intact arterial blood flow should raise a red flag for all EMS providers.

Assessment and Recognition

The patient with crush injury may initially present with few signs or symptoms.

EMS personnel should maintain a high index of suspicion when treating victims with the potential for CS/CI. If treatment is delayed while waiting for the patient to present with clinical signs, the window for optimal outcome may be lost. CS/CI management therapies should be considered early in the case of an anticipated prolonged extrication or in an extreme case.

CS/CI should be suspected in patients with a high probability of compression-type injuries or prolonged exposure to constant pressure. Most patients who develop CS/CI have extensive injuries involving a lower extremity and/or the pelvis. For development of systemic signs and symptoms, the injury must generally involve more than just one hand or one foot. Also, the crushing force must be present for some time before CS/CI can occur. The syndrome may develop after one hour in a severe crush situation, but it usually takes four to six hours of compression for the processes that cause crush injury syndrome to occur. This does not mean, however, that treatment should be delayed. A strong clinical picture and suspicion for CS/CI should force consideration of a CS/CI management protocol.

Physical findings common to the CS/CI patient include a tense or tight feeling to the skin surrounding an extremity. This tension should be of concern and warrants transport to a trauma center. If the skin is stretched enough to create a tight feeling, the patient will likely require immediate surgical intervention.

Hallmark signs experienced by the CS/CI patient include the "5 P's": pain, pallor, paresthesia, poikilothermy (cold skin) and pulselessness. If the patient has a clinical history suggestive of CS or CI, coupled with any or all of the five P's, there is a high likelihood he requires immediate evaluation at a trauma center.

Management

If prolonged extrication is expected, or there is a history of four or more hours of downtime, treat the patient for CS/CI. Do not wait for clinical signs to develop, as the patient may already be in renal failure and the degree of metabolic acidosis will worsen. As with all significant trauma patients, manage the airway and ventilation if necessary, administer oxygen at a high concentration, and apply a continuous ECG monitor for cardiac dysrhythmia recognition.

BLS Care

One of the primary considerations in BLS management of CS/CI patients is the coordination of compartmental release by rescue personnel. If a patient is trapped, the instant the pressure is released, reperfusion will occur and the release of toxic substances will ensue. If the BLS provider is cognizant of the events following release of pressure, ALS support can be attained to mitigate the effects of reperfusion or a venous tourniquet can be applied to slow the effects. Tourniquet use is controversial, however, and should only be done in conjunction with medical direction.

In addition to controlling reperfusion, BLS providers must also maintain the patient's core body temperature. Splinting the limb at heart level is important, because it will help limit edema and maintain perfusion. Another consideration must be management or prevention of shock. Finally, a victim of CS/CI must be transported rapidly to an appropriate trauma center, in some cases by aeromedical transport. As soon as a CS/CI is suspected and extrication is expected to be prolonged, ALS backup should be initiated.

ALS Care

Maintain high kidney output by hydrating the patient with crystalloid IV fluids to minimize the potential for obstructed renal tubules. Normal saline is the solution of choice over lactated Ringer's in the prehospital setting because it does not contain potassium. Intravenous fluids will dilute the concentration of myoglobin and keep the kidneys working. Remember that CS/CI are often very painful and warrant administration of pain management medications as early as possible and when appropriate.

Administration of sodium bicarbonate is one of the most beneficial prehospital treatments for several reasons: it will aid in reversing any pre-existing metabolic acidosis; it will provide an initial benefit in the treatment of hyperkalemia; and, it will keep the urine alkalotic, which may prevent renal tubule obstruction. The initial CS/CI dosage for sodium bicarbonate is 1.0 mEq/kg IV bolus, repeated at one-half the initial dose after 10 minutes, or, preferably, 50-100 mEq/1000 cc of .9NS run at 150 cc/hr.

Mannitol is thought to be a useful medication in promoting diuresis of the circulating volume to reduce urine acidity. Lasix, however, should not be administered, because it makes urine acidic and may actually worsen the condition. Also, the site of renal obstruction is typically in the lower tubules, below the loop of Henle where Lasix exerts its action. Mannitol can be given in doses of 1 gm/kg or added to the patient's intravenous fluid as a continuous infusion, with a maximum dose of 200 grams per day, since higher doses may cause renal failure. Mannitol should only be administered after good urine flow has been established following IV hydration.

As the patient progresses through the hospital phase of treatment, hyperbaric oxygen (HBO) therapy, which has been proven effective in treating CS/CI, may be considered. If the pressure does not resolve, an open fasciotomy into the injured compartment may be performed to allow underlying muscles to swell without impeding blood flow. If all else fails, amputation of the extremity may be necessary to prevent spread of tissue necrosis and infection.

Objectives

• Review pathophysiology of crush injury and compartment syndrome
• Discuss prehospital assessment and management of these conditions

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William S. Krost, BSAS, NREMT-P, is an operations manager and flight paramedic with the St. Vincent/Medical University of Ohio/St. Rita's Critical Care Transport Network (Life Flight) in Toledo, OH, and a nationally recognized lecturer.

Joseph J. Mistovich, MEd, NREMT-P, is a professor and chair of the Department of Health Professions at Youngstown (OH) State University, author of several EMS textbooks and a nationally recognized lecturer.

Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, ME. He is the author of several EMS textbooks and a nationally recognized lecturer.