Crush Injuries and Compartment Syndrome

Prehospital Pathophysiology is a new monthly column that provides an opportunity for EMS providers of all levels to either refresh their knowledge related to the etiology of a certain disease or expand their knowledge base regarding common and not-so-common disease processes. This column is for both basic- and advanced-level prehospital care providers. The authors hope that through this column, EMS providers will gain a more thorough understanding of disease processes. If you would like to see a specific topic addressed in this column, send your request via e-mail to emseditor@aol.com.

Pathophysiology

Crush injury (CI) and compartment syndrome (CS) are different processes with very similar pathophysiology and 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 is defined as any condition in which a structure like a nerve or tendon has been constricted within a space. Compartment syndrome is most 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 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. This leads to restricted blood flow because capillaries are compressed by the pressure. 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 has been 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 beat effectively. In a crush injury, this same principle of pressure applies. As pressure builds within an extremity, the skin will only stretch so far. Eventually, the pressure will be transferred from the skin to the vessels and internal structures of the extremity.

Although trauma is the most likely cause of CS/CI, they can occur in nontraumatic situations. A stroke patient who is found after lying motionless on his arm for several hours could have an unidentified compartment syndrome.

The most prominent type of muscle in the body is skeletal muscle. The skeletal muscle cell membrane, also known as the sarcolemma, is a key factor in ensuring normal cell function and maintaining a normal cell structure. The cell membrane contains pumps that move potassium and calcium to the inside of the cell and sodium to the outside. These pumps rely on energy in the form of adenosine triphosphate (ATP). Myoglobin, which is found within the skeletal muscle cell, is responsible for supplying the 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 so it may be used in normal cell metabolism. The skeletal muscle cell also contains enzymes that are not harmful to the cell itself unless the calcium level in the cell rises. When the calcium level rises, the enzymes become destructive to the cell structure and cause the cell membrane to leak or rupture.

Damage to the skeletal cell membrane, both from direct injury or the loss of energy and dysfunction of the cell membrane pumps, causes calcium and sodium to rush inside the cell, and causes substances such as myoglobin, potassium, uric acid and phosphorus to leak out of the cell. These substances are leaked into the interstitial fluid (fluid around the cell) and may be eventually 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, a protein that 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. This leads to systemic effects of compartment syndrome because the kidneys are unable to filter the large myoglobin molecule. This may completely obstruct blood flow to the kidneys, leading to kidney failure and death.

In either type of injury, compression occurs and venous blood flow is impeded to an extremity. In a normal, healthy patient, the venous system allows blood to leave the extremities, thereby removing carbon dioxide and waste products from the body. These types of injuries are problematic because, although venous flow is stopped, arterial flow is not, and significant pressure begins to build within the injured tissue.

The lack of oxygenated blood flow 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 development of metabolic acidosis in the extremity.

Once the blood flow obstruction is corrected and blood is able to flow out of the extremity, the toxic substrates that have been forming within the tissues of the extremity are released into the patient's systemic circulation. When these substrates (chemicals) come into contact with healthy tissues, the patient may become metabolically acidotic. A side effect of metabolic acidosis is widespread vasodilation, which may induce a period of relative hypovolemia because the patient is vasodilated but maintains an adequate fluid volume. Consider the effects that the high levels of potassium and the acidotic blood will have on the heart once they are released. Assuming an injury is present and potassium levels are high enough, there is a good chance that the patient will die due to the acid-base and electrolyte imbalances pres­ent within the heart. Ventricular fibrillation is the most commonly seen arrhythmia in CS/CI patients who experience sudden cardiac death.

As potassium rushes into the systemic circulation, myoglobin is also rushing into the vasodilated tissue. Normally, a release of myoglobin in the tissue is not detrimental, because myoglobin is soluble in blood with a normal pH level. It has already been established that the pH of a patient with a crush injury will likely be acidotic. Hence, the rapid flow of blood and the large myoglobin molecules often promote renal failure.

Recognizing a crush injury or compartment syndrome is highly dependent on obtaining an accurate clinical history and, to some degree, the patient's 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 & Recognition

The physical findings common to CS/CI include a tense or tight feeling to the skin surrounding an extremity. This tension should be of concern and would warrant transporting the patient 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 what is commonly referred to as the "Five Ps": pain, pallor, paresthesia, poikilothermia (cold skin) and pulselessness. If the patient has a clinical history suggestive of CS or CI, coupled with any or all of the five Ps, there is a high likelihood the patient requires immediate evaluation at a trauma center. In the hospital, Doppler studies of the extremity may be performed, or a needle attached to a pressure gauge may be inserted into the extremity at various points to obtain pressure readings within the extremity and identify differences in pressures.

Management

In patients with suspected CS/CI, and all significant trauma patients, administer oxygen at a high rate of flow and monitor for cardiac dysrhythmias. Maintain high kidney output by hydrating the patient with crystalloid IV fluids to minimize the potential for obstruction of the renal tubules. Admini-stration of IV fluids will help to dilute the concentration of myoglobin and keep the kidneys working. Administering sodium bicarbonate may be helpful, as it will keep the urine alkalotic and may prevent renal tubule obstruction. Mannitol is thought to be helpful in diuresing some of the circulating volume to reduce the acidity of the urine. Lasix is inappropriate, as it may worsen the condition. In addition to making the urine acidic, Lasix is ineffective because the site for renal obstruction is typically in the lower tubules, below the loop of Henle. 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; the patient may have already begun to go into renal failure, and the degree of metabolic acidosis will worsen.

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

Bibliography

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