Extent of traumatic injury can be determined by three factors: energetics, mechanism, and anatomic region.

The energetics are determined by the basic physical principle that kinetic energy is directly proportional to mass and square of velocity. The relevant mass and velocity are those of the offending object, and the transfer of energy (and consequent potential for injury) depends on the mass and density of the injured body region. More extensive injuries can occur with high-velocity bullets and bullets that tumble upon entry, causing a “dim-dum” effect. The wounds caused from these missiles show characteristic small entrance wounds, with a large amount of tissue loss due to a cavitation effect upon entry. This is attributable to a more efficient dissipation of energy from the bullet to the surrounding tissues. The increased tissue loss and injury to collateral vessels can lead to a more severe degree of ischemia in these injuries. Another special circumstance occurs with injuries due to shotgun blasts. At close range, there is a large amount of soft tissue injury and collateral vessel damage. These wounds are more likely to become infected, and embolization of the shot is occasionally seen.

Mechanisms of injury are classified as either penetrating or blunt. The majority of penetrating injuries in the civilian population are due to knife wounds or low-velocity gunshot wounds. However, with the spread of assault rifles into the civilian population, high-velocity gunshot wounds are now increasingly frequent. As previously mentioned, the degree of vascular injury associated with these weapons is high. Blunt trauma is usually associated with motor vehicle accidents or falls from a height. However, it should be remembered that any mechanism associated with blunt force could result in a vascular injury. Blunt injury results from stretching or compression of the vessel, often associated with bony fractures or dislocations. This is especially true near joints, as the vessels are usually relatively fixed in these locations. Bony fracture may also generate shards of bone, which may produce a secondary penetrating injury to the vessel. In addition, deceleration injuries may cause injury at sites where the artery is relatively fixed. An example of this is aortic disruption, seen frequently at the ligamentum arteriosum or at the level of the diaphragm.

Certain anatomic locations are more prone to vascular injuries. While these specific injuries will be considered in the ensuing chapters, some important examples include aortic injury with deceleration trauma, carotid or vertebral injury with flexion/extension injury, brachial artery injury associated with proximal humeral fracture, common femoral/external iliac injury secondary to needle or catheter access, and popliteal injury following posterior knee dislocation, supracondylar fracture of the femur, or tibial plateau fracture.

The immediate consequence of vascular injury is ischemia distal to the site of injury. This is more pronounced in blunt injuries and high-velocity penetrating injuries, as there is more diffuse tissue trauma, increasing the likelihood of injury to collateral vessels. By about 6 hours of warm ischemia time, myonecrosis begins to develop. This so-called “golden period” for revascularization and prompt restoration of flow should always be a priority for the surgeon. Reversal of ischemia can result in reperfusion injury, which is characterized by the generation of oxygen free radicals, inflammatory cytokines, and the migration and activation of inflammatory cells. A secondary injury can then occur within the reperfused region, resulting in the disruption of cellular membranes, cell death, and extravasation of fluid into the surrounding tissues. Within the extremity, elevated interstitial pressure in a region bounded by fascial planes can block venous outflow, leading to increased congestion and tissue pressure, which causes its own ischemic effect. Surgical treatment of compartment syndromes will be separately discussed in this text. Systemic effects of the reperfusion syndrome can also be manifest, depending on the degree of tissue ischemia and the volume of tissue affected. This is largely due to circulating inflammatory mediators, acidosis, hyperkalemia, and myoglobinemia. Organ system involvement includes acute renal failure, myocardial depression or cardiac
dysrhythmias, and the acute respiratory distress syndrome.

Care of the patient with vascular trauma generally begins with presentation to the emergency department of a trauma center. Pertinent historic details include mechanism (penetrating, blunt, or combined), approximate time since injury, blood loss at the scene (arterial or venous), and known prior disabilities/injuries. In penetrating injuries, other important factors include the type of weapon used (e.g., length of knife, caliber of bullet), number of entrance/exit wounds, and body position at the time of injury. In blunt force trauma, pertinent factors include the height of the fall, the speed of the automobile at time of impact, time of extrication, evidence of steering wheel compression or seatbelt injury, and other fatalities at the scene. While this information can be helpful in the trauma assessment, it is often not readily available, and its determination should not delay further treatment.

At this point, initial assessment and management follow the protocols of Advanced Trauma Life Support as set forth by the American College of Surgeons Committee on Trauma. Priority assessments in this algorithm begin with the classic “ABCs”: airway, breathing, and circulation. Securing a safe airway may require surgical intervention, which can be accomplished by cricothyrotomy or emergency tracheostomy. Expanding hematomas in the neck may also hinder intubation using standard orotracheal techniques. If possible, controlled fiberoptic intubation in the operating room should be performed. Once the airway is secure, attention is turned to ensuring adequate pulmonary ventilation (i.e., gas exchange). Ventilation may be compromised due to hemothorax caused by intercostal vessel laceration or by a thoracic vascular injury. Upright chest x-rays can provide initial assessment for mediastinal injury or for blood within the pleural cavity. This should be treated by tube thoracostomy or appropriate surgical intervention. Next, circulation is assessed with awareness of the role of vascular injury on blood pressure.

In a supine patient, a palpable carotid or femoral pulse indicates a systolic pressure of at least 60 mmHg, and a palpable femoral pulse correlates with a pressure of 90 mmHg. Significant hypotension must obviously be addressed with a search for gross cardiac dysfunction or a site of significant exsanguination. Voluminous bleeding can generally be controlled best with pressure either directly at the wound or at the proximal arterial supply. This may require placement of an arterial tourniquet, though this practice is considered extreme and should be used to temporize until the patient can be transported to the operating room and proper surgical control achieved.

The best overall patient outcome from serious trauma will result from timely surgical repair in a patient who is properly resuscitated. Rapid efforts should be made to oxygenate the patient well and resuscitate toward correction of hypotension. This is a common problem in the trauma victim, and surgical trauma care leans toward liberal provision of intravenous fluids. But surgeons and anesthesiologists on the trauma team are cautioned not to be capricious in fluid resuscitation. Whereas physicians’ instinct is to aim for a normovolemic, normotensive state, there is increasing support in clinical experience and laboratory research to demonstrate the virtue of permissive hypotension. Volume resuscitation to a goal pressure of 130 mmHg may lead to dislodgement of an initial hemostatic plug and may only encourage further bleeding. This can then result in a vicious cycle of further transfusion and increased intravascular pressure, resulting in more hemorrhage, subsequent pressure loss, and more transfusion. Tolerance of systolic pressures of 90 mmHg may be more appropriate in a trauma victim, as long as this does not appear to cause end-organ dysfunction (e.g., oliguria).

Selection of resuscitation fluid is another important option in the medical management of a trauma victim. ATLS guidelines recommend beginning with two liters of crystalloid solution. Isotonic fluids, such as normal saline, or resuscitative, buffered solutions, such as Ringer’s lactate or Plasmalyte, are the recommended fluids, because they function as volume expanders. Persistent hypotension and/or anemia may prompt the transfusion of packed red blood cells, and there is unquestionable wisdom to this decision in selected patients. However, several contemporary clinical trials have challenged historic guidelines, such as transfusion for hematocrit less than 30%. Cumulative effects of transfusion appear to have untoward effects on the immune system, and more frequent transfusion is correlated with worse long-term outcomes. Therefore, higher transfusion thresholds, tolerating hematocrit ≤21% to 25% or ≤27% to 30% in patients with heart disease, may lead to superior overall patient outcome.

Two other general options exist: synthetic colloid solutions and oxygen-carrying fluids. Colloid solutions such as albumin, dextran, or hetastarch have a theoretic advantage of remaining intravascular and limiting pulmonary edema and peripheral edema. However, these benefits have never been proven in clinical trials, so there is no convincing benefit to using these fluids over crystalloids. Given their increased cost and potential for allergic reactions, they are generally not used except in hypoproteinemic patients, such as those with hepatic cirrhosis. Years of re-search have gone into developing a nonblood oxygen-binding solution to improve tissue oxygen delivery without the risks and potential harmful effects of blood product transfusion. The major difficulty with developing such compounds has been developing solvents with the remarkable cooperative behavior of hemoglobin, which allow it to take up oxygen in the pulmonary vasculature and then unload it in oxygen-starved tissues. Developing polymerized bovine hemoglobin solutions has proved effective in animal models, but more research and clinical trials are required before these agents become a standard part of the clinician’s armamentarium.

Other general concerns of aggressive transfusion include exacerbation of chronic medical conditions, most notably congestive heart failure and renal insufficiency. Patients in these populations are especially susceptible to complications of hypervolemia, and care must be taken in their hydration and resuscitation. However, the demographics of the trauma patient population center on healthy young men, so these issues are not commonly of concern. Nevertheless, the skilled trauma surgeon designs a patient’s care based on their specific characteristics and physiology.

It is also important to remember that hypotension in the setting of trauma may be caused by problems other than hypovolemia, such as intoxication, neurologic injury, or cardiac dysfunction. In a trauma victim, the latter may be acutely caused by myocardial contusion, pericardial constriction, or ischemia from coronary dissection.

During the secondary survey, physical exam findings that suggest vascular injury must be carefully sought. A thorough head-to-toe physical examination should
be performed, to document relevant deficits and identify occult injuries. Pulses should be assessed in the neck and extremities. However, the presence of a pulse does not completely rule out arterial injury, as a palpable pulse may be felt in up to 33% of cases. A transmitted pulse wave may be propagated through thrombus or collateral vessels, yielding a distal pulse. As this pulse wave is slowed in transmission (7 to 13 meters/second), the pulse may be delayed or attenuated. An audible bruit or a palpable thrill may be detected, signifying a possible arteriovenous fistula. A well-documented neurologic exam is critical, as associated nervous injury is reported in 18% of arterial injuries. Bony deformities, fractures, or dislocations should raise the suspicion of underlying vascular damage. Skin changes should also be documented, especially in the assessment of hypovolemic shock. Asymmetry of skin changes between extremities may herald an underlying arterial injury.

Signs of arterial injuries are traditionally described as “hard” or “soft.” Hard signs should impart high suspicion of vascular injury. These include external arterial hemorrhage, expanding and/or pulsatile hematoma, pulselessness, paresthesia, paralysis, poikilothermia, palpable thrill, audible bruit, and general evidence of ischemia. Soft signs should signal intermediate suspicion of vessel injury: diminished distal pulses, proximity of penetrating injury or fracture to known vessels, previous (venous) bleeding at the accident scene, and peripheral neurologic deficit. These classifications can be somewhat artificial, and suspicion of arterial injury should be based on clinical judgment. However, classification of injuries in this way can be helpful in the triage of patients to further diagnostic tests, immediate operation, or continued observation.

Signs specific to different anatomic locations will be discussed in subsequent chapters. However, the pre-operative assessment of extremity injury deserves special consideration. In lower-extremity injuries, a very useful means of quantifying the lower-extremity pulse exam is the ankle-brachial index (ABI). By measuring blood pressure in all limbs using a Doppler and blood pressure cuff, a ratio of arm-to-leg blood pressure can be obtained. An ABI below 0.9 suggests vascular compromise. However, this measurement does not take into account the presence of pre-existing peripheral occlusive disease. For this reason, an arterial pulsatility index (API) is used in determining traumatic injury. The API is defined as the ratio of systolic blood pressure of the affected extremity over the unaffected extremity. An API of < 0.9 is reported to have a 95% sensitivity and 97% specificity in detecting arterial injuries in the extremity. However, false negatives do occur, as the API will miss venous injuries and injuries to nonconduit vessels (e.g., profunda femoris artery). The reported negative predictive value of an API greater than 0.9 is 99%. We recommend that an API < 0.9 should elicit further diagnostic testing.

Plain radiographs are essential in the basic trauma evaluation. Routine radiographs include cervical spine evaluation, upright chest x-rays, and abdominal and pelvic views. These films may also document the presence of radio-opaque foreign bodies, such as bullets or shrapnel. Bullets that have migrated beyond the trajectory defined by the entrance and exit wound raise the possibility of a bullet embolus. All suspected orthopedic injuries should be addressed by appropriate radiographs to diagnose fractures and dislocations.