Injury to a major peripheral artery can be limb threatening. If active hemorrhage is present and not urgently controlled, vascular trauma can be life threatening. In either case, diagnosis and management must be expeditious. This chapter reviews the epidemiology, pathophysiology, clinical presentation, management, and outcome of extremity vascular injuries.

Vascular injuries of the extremities are not very common. In urban trauma centers, peripheral vascular injuries are present in less than 5% of admissions; in rural centers they are even less common, occurring in 1% of admissions.^1,2 Most are penetrating and occur predominantly in males in their third and fourth decades. Blunt trauma sufficient to produce fractures or dislocations, handguns, and knives cause the vast majority of civilian extremity vascular injuries. High-velocity projectiles and shrapnel are the predominant wounding agents in the military experience.³

Because of the increase in endoluminal procedures, the number of iatrogenic arterial injuries increased 40% between 1996 and 2003.⁴ Iatrogenic arterial injuries occur in approximately 0.6% of patients undergoing endoluminal therapies and appear to be specialty related. Most of these injuries involve the groin where access is most commonly obtained for interventional procedures. Iatrogenic vascular injuries can also occur during open operations on the extremities, such as during total joint procedures, intramedullary and external fixation, and during plate osteosynthesis. They can present as hemorrhage or ischemia during the procedure or immediately after (usually in the recovery room) or they can present months or years later as claudication or acute limb threatening ischemia due to thrombosis or emboli.⁵ They are definitely not benign; a recent report documented a 5.2% mortality following iatrogenic injury.⁶

Arteries and veins are composed of three tissue layers: the outer adventitia of connective tissue, the central media of smooth muscle and elastic fibers, and the inner intima or endothelial cell layer. Trauma to a blood vessel (artery or vein) can produce hemorrhage, thrombosis, or spasm, either alone or in combination, depending on the mechanism and the magnitude of the force applied to the vessel. Hemorrhage occurs when there is a laceration or puncture of all of three layers. If the bleeding is tamponaded by the surrounding tissue (ie, muscle or fascia), a localized hematoma will form, which may be pulsatile. If local tamponade is ineffective, or only temporarily effective, immediate or delayed hemorrhage ensues, which can be life threatening. Damage solely to the intima occurs when an artery is acutely deformed or angulated. The intima is the least compliant of the vascular layers and it fractures when the more flexible layers bend when deformed by an adjacent broken bone or joint dislocation. Intimal injury exposes the subendothelial matrix, which is rich in tissue factor, resulting in activation of the clotting cascade and subsequent thrombus formation. The thrombus may enlarge or propagate and occlude the vessel or embolize and produce a distal occlusion. The injured intima may also form a flap that can prolapse into the arterial lumen as a result of the forward blood flow dissecting under it. The prolapsed intima can partially or completely obstruct the lumen. Displaced bone from a fracture or dislocation can compress a vessel to the point of completely interrupting flow. Stretching or contusing an artery can produce spasm or segmental narrowing (Fig. 41-1). Bleeding adjacent to a vessel also produces spasm due to the vasoconstrictive effects of hemoglobin on the external surface of an artery.⁷ Spasm that reduces a vessel diameter by 50% will reduce the cross-sectional area by 75%, which is sufficient to significantly reduce distal flow.

Penetrating injuries produce focal injury, while blunt injuries tend to be diffuse and injure not only the vascular structures, but also the adjacent bone, muscle, and nerves. This adjacent tissue contains small, unnamed vessels that would normally provide collateral flow around an injured named vessel. This “collateral” damage worsens or exaggerates existing ischemia.

Velocity, rather than size, matters in penetrating injury because the energy imparted to a target by a projectile is equivalent to one-half the mass of the projectile multiplied by the velocity of the projectile squared. As a result, penetrating mechanisms are classified as either low velocity (<2500 feet per second [ft/s]) or high velocity (>2500 ft/s). Low-velocity wounds include stabs, fragment injuries, and low-velocity gunshot wounds. High-velocity (>2500 ft/s) wounds are most commonly inflicted by a military assault rifle. Because of the imparted kinetic energy, high-velocity weapons are capable of producing significantly more tissue damage than low-velocity weapons.

Peripheral vascular injuries can be subtle and go undetected. Symptoms or signs may not be present during the initial phases of care or even during the initial hospitalization. With time, however, they progress insidiously and eventually produce signs and symptoms. The most common of these indolent injuries are the arteriovenous fistula and the pseudoaneurysm. An arteriovenous fistula typically occurs after penetrating trauma that causes a puncture or small laceration to both an artery and an adjacent vein. The high-pressure flow from the artery will follow the path of least vascular resistance into this adjoining vein. Because the fistula is small initially it is undetected, but with time it enlarges diverting nutrient flow from the distal vascular bed. As it enlarges it produces local, regional, and systemic signs and symptoms (Fig. 41-2). These include local tenderness and edema, regional ischemia from “steal,” and congestive heart failure if the involved artery and vein are major conduits.⁸ A pseudoaneurysm is a result of a puncture or laceration of an artery that bleeds into and is controlled by the surrounding tissue. The artery remains patent; blood flows into and out of the pseudoaneurysm—much like the ebb and flow of ocean water into and out of a tide pool. As a pseudoaneurysm enlarges it can produce local compressive symptoms, erode adjacent structures, or, rarely, be a source of distal emboli.

Some peripheral arterial injuries heal without an intervention. It has been convincingly demonstrated that most asymptomatic vascular injuries have a benign natural history and either completely resolve or remain stable. Dennis and colleagues have demonstrated that small intimal flaps, intimal “irregularities,” small pseudoaneurysms, and small arteriovenous fistula can heal with little residual deformity.⁹ It is impossible to predict which of these lesions will heal, which will progress, but remain asymptomatic, and which will eventually develop either acute or chronic symptoms. For this reason, close follow-up with periodic duplex color flow imaging is essential.

A reduction in blood flow from an arterial injury to the extent that the oxygen demands of the tissue supplied by that artery are not being met produces ischemia. The vulnerability of a tissue to ischemia depends on its basal energy requirement, substrate stores, and duration and severity of the ischemic insult. Peripheral nerves are most vulnerable to ischemia because they have a high basal energy requirement and virtually no substrate (glycogen) stores. Therefore, sensory deficits are often the first manifestations of vascular injury that produces ischemia. Skeletal muscle is more tolerant of decreased blood flow; histologic changes are not evident unless ischemia has been present for 3 hours or more. In a porcine model, functional derangements and histologic change in both nerve and muscle occur in 3 hours following onset of ischemia even if reperfusion is established by the end of that interval.¹⁰ The more complete the interruption of arterial inflow, such as occurs with occlusion of a major arterial conduit and disruption of collateral vessels, and the longer the duration of interrupted flow, the greater the potential for irreversible ischemic damage.

After prolonged complete ischemia, damage can be extended rather than reversed by reperfusion. This ischemia/reperfusion injury is thought to be initiated by hypoxic disruption or “shedding” of the endothelial glycocalyx, which changes the normal endothelial cell phenotype from anticoagulant and anti-inflammatory to procoagulant and proinflammatory.¹¹ Recent evidence suggests that both the complement and kinin cascades are triggered, which exacerbate the injury by attracting neutrophils. In addition, vascular integrity is lost resulting in interstitial edema. Interstitial edema raises the interstitial fluid pressure eventually occluding venules, capillaries and arterioles and resulting in the “no reflow” phenomenon, compartment syndrome, and myonecrosis or rhabdomyolysis with release of myoglobin and potassium from the irreversibly injured myocytes.¹¹ Myoglobin is nephrotoxic and hyperkalemia, if untreated, can lead to a fatal arrhythmia.

There are a several factors that are important in determining the outcome of extremity vascular injury. The factor of greatest importance, based on an understanding of the pathophysiology of ischemia and reperfusion, is the elapsed time from injury to restoration of flow. Notice that it is the elapsed time from injury, not hospital arrival that is critical and it is the time to restoration of flow, not completion of the arterial repair. Because the time of injury is not always exactly known, it is best to estimate a longer prehospital interval than a shorter one and let this govern the urgency with which management occurs. Based on recent experimental work using a model of complete vascular occlusion,¹⁰ restoration of flow within 3 hours appears to be optimal to avoid any ischemic changes in nerve and muscle. A delay of greater than 6 hours from injury to restoration of flow results in myonecrosis and moderate Wallerian degeneration of the peripheral nerves.

Other factors that can adversely affect limb salvage and limb function following both upper and lower extremity vascular injury include blunt mechanism, the presence of hypovolemic shock, associated nerve injury, associated orthopedic injuries, and associated comorbidities. All of these factors being similar, the upper extremity appears to be more tolerant of ischemia, which is likely due to relatively better collateral flow around the shoulder and elbow joints.^12,13

The presentation of extremity vascular injury varies from obvious life-threatening external hemorrhage from penetrating injury to ischemia from blunt force trauma. As stated previously, penetrating extremity trauma tends to be focal and most frequently is unaccompanied by other injuries. The same is not true for blunt trauma, which is more diffuse and often associated with multiple injuries. For penetrating focal injury it is important to obtain a history from the prehospital providers regarding the approximate time of injury, the agent (ie, stab wound, gunshot wound, etc) and the amount of blood lost at the scene and during transport. For blunt trauma additional history should include a description of the mechanism of injury (ie, pedestrian stuck, rollover with ejection, etc), and, in the case of motor vehicle crashes, the amount of damage done to the vehicle. This information allows the physician to estimate energy transfer—the greater the energy transfer the higher the index of suspicion should be for occult vascular injury, not only in the extremity, but also in the torso. Fracture and dislocation patterns often suggest the possibility of extremity vascular injury. For example, in the upper extremity, a supracondylar fracture of the humerus can be associated with a brachial artery injury. Similarly, in the lower extremity, posterior knee dislocation can be associated with a popliteal artery injury.

The presence of unexplained hemorrhagic shock in patients without evidence of head, neck, or torso injury should direct attention to apparently trivial extremity lacerations. This is particularly important in wounds in the antecubital fossa, groin, and popliteal fossa where initial hemorrhage from a laceration of the deep vessels may have led to hypotension and subsequent thrombosis.

With the above in mind, the following sequence of steps is strongly recommended: primary survey as described by the Advanced Trauma Life Support Course (ATLS), control ongoing hemorrhage by compression or the use of a proximal tourniquet if compression is unsuccessful,^3,14,15,16 followed by a secondary survey as described by ATLS with focus on the injured limb (see below), and a repeat ATLS primary survey.

History and Physical Examination

The history and physical examination are the initial critical steps in the diagnostic evaluation of a patient with a potential extremity vascular injury. The history (obtained from either the patient or the prehospital providers) must include the mechanism and the time elapsed since injury. In addition to obtaining a list of medications (as well the use of illicit drugs with vasoconstrictive properties, such as cocaine and methamphetamine) and preexisting diseases in patients over the age of 50, a history of claudication in either or both lower extremities must be sought and documented. The physical examination must include vital signs—including systolic blood pressure and temperature, both of which can affect the extremity vascular exam. Hypotension causing peripheral vasoconstriction will reduce or eliminate the peripheral pulse in an uninjured limb; hypothermia will prolong capillary refill. Therefore, resuscitation and rewarming may improve the pulse exam in the limb without a vascular injury, but will have little or no effect in the limb with a vascular injury. Extremity dressings should be promptly removed to assess and document the nature of the underlying wounds. The following should be noted and documented if present or absent (negatives are pertinent for subsequent examinations): active bleeding, hematoma (including whether it is soft or tense), bruit, or thrill. Examination of the uninjured contralateral extremity, in our practice, usually precedes that of the injured limb; the uninjured limb provides the basis for comparison. This includes a vascular and neurologic examination (sensory and motor) with careful palpation of peripheral pulses, assessment of color, warmth, capillary refill and venous filling. The vascular and neurologic findings in the injured and the uninjured limb must be accurately documented. This provides important information necessary for follow-up examinations—both preoperatively and postoperatively. There is an unfortunate tendency to “overcall” the presence of peripheral pulses. Once any examiner documents that a pulse is present when it is, in fact, absent, there is a tendency of subsequent examiners to do the same. When in doubt, declare the pulse absent and proceed to the use of a continuous wave (handheld) Doppler device. Venous signals can be heard and mistaken for an arterial signal; venous signals augment with distal compression; arterial signals do not. The experienced examiner can assess flow based on the character of the audible Doppler signals. However, when there is an abnormal (absent or reduced) pulse, the arterial pressure index (API) should be determined.¹⁷ The manual blood pressure cuff is placed just proximal to the wrist or ankle in the injured extremity and the probe is placed over the distal vessel. The cuff is slowly inflated and the cessation of the arterial signal indicates the systolic blood pressure at the level of the cuff. The uninjured contralateral extremity and an uninjured arm pressure are then determined. The normal ankle–brachial index is 1.1. Unless the patient has preexisting peripheral vascular occlusive disease, the ankle–brachial index should be at least 0.9 and there should be less than a 20-mm Hg difference between the two lower extremities. An absolute pressure below 50–60 mm Hg at the wrist or ankle indicates limb-threatening ischemia in the patient with a normal systemic blood pressure. The API is not useful in patients with advanced diabetes in whom the proximal conduit arteries are severely calcified making them noncompressible, even at high cuff inflation pressures.

There are very distinct physical findings that clearly indicate a vascular injury (Table 41-1). In addition to these “hard signs,” there are less obvious but equally important “soft signs” that suggest the possibility of extremity vascular injury. The hard signs indicate a high probability of vascular injury requiring surgical repair.¹⁸ Expanding hematoma, hemorrhage, and ischemia require immediate exploration, while a bruit or a thrill, in the absence of hemorrhage or ischemia, is best addressed after vascular imaging. The presence of any one of the soft signs mandates vascular imaging.

Vascular Imaging

The advent of high-resolution multidetector CT angiography (CTA) has radically changed the approach to contrast imaging for extremity vascular trauma. Catheter arteriography used solely for the diagnosis of a potential vascular injury has been replaced by CTA. Multidetector (64 slice) CTA with the appropriate imaging protocols creates axial, coronal and sagittal views within minutes.^19,20 The latest software produces 3D reconstructions without the need of delays associated with workstation manipulations. In addition to being very accurate, CTA avoids not only the delay necessary to assemble the angiography team, but also the potential complications associated with arterial access. Catheter arteriography is now reserved for those patients with suspected vascular injury in whom a catheter-based therapy may be necessary (see the section “Endovascular Management”) or for those patients with blast injuries or shotgun wounds in whom metallic fragments or pellets can produce artifacts on the CTA that obscure the arterial or venous lumen. The indications for vascular imaging have not changed (Table 41-2).

In the patient who is neurologically or hemodynamically unstable, a single-injection arteriogram in the trauma room or operating room is a quick and accurate method to evaluate an extremity with a suspected vascular injury (Table 41-3).²¹

Noninvasive Evaluation

Color flow ultrasound imaging is useful for the diagnosis of chronic vascular injuries, such as a pseudoaneurysm or an arteriovenous fistula, and for the postoperative follow-up of vascular repairs. It has not proven useful in the diagnosis of acute arterial injury because it requires the presence of a skilled vascular technologist to perform the test and an experienced provider to interpret the study—neither of which is usually available on an expedient basis. In those patients with severe renal insufficiency in whom the use iodinated contrast might precipitate permanent renal failure, duplex scanning, with the caveats noted previously, combined with a thorough physical examination can be used to rule out an arterial injury. If doubt remains the calculus of harm must be assessed with respect to the risk of a contrast study versus that of an operative exploration.

Practice Recommendation for Extremity Vascular Diagnostic Evaluation

The recommended diagnostic approach is detailed in Fig. 41-3. Physical examination remains the most important element of this process. Common sense dictates that those with obvious injury go directly to the operating room to delineate and repair the injury. Imaging with either high-resolution CTA or catheter arteriography must make sense in terms of the expense of time and the value of the results in deciding and directing the management.

Minimal Vascular Injury and Nonoperative Management

Minimal vascular injuries are those that are asymptomatic and have the potential to heal without becoming symptomatic. The diagnosis is made following imaging obtained for suspected vascular injury manifested by the soft signs. Minimal vascular injury includes intimal irregularities (ie, intimal flap), small arteriovenous fistulae, focal spasm with minimal narrowing, and small pseudoaneurysms.²² Progression of these lesions to produce symptoms occurs in approximately 5–15%⁹ and usually occurs early in the post-injury course. Considerable evidence suggests that nonoperative therapy of these asymptomatic lesions is safe and effective.²² The possibility of progression, while remote, necessitates compulsive inpatient and outpatient follow up with repetitive physical examinations (including the API) and the liberal use of color flow imaging. Operative therapy is required for thrombosis, ischemia (including ischemic “steal” produced by an enlarging arteriovenous fistulae), and failure of small pseudoaneurysms to resolve.

Endovascular Management

The use of endovascular therapies for extremity vascular injuries is increasing. These therapies include branch coil embolization, vasodilator infusion, and the use of covered and uncovered stents. There are now several small retrospective case series and a single prospective report describing the use of covered stents for the treatment of chronic injuries, such as arterial pseudoaneurysms and arteriovenous, and acute injuries with hemorrhage, dissection and thrombosis.^3,23,24,25 The most common injuries treated acutely are those involving the subclavian and axillary arteries, probably due to the relative difficulty in open operative exposure of these two arteries. The evidence to support endoluminal therapies for peripheral injuries remains parochial, as there is no consensus on the indications, no uniform definitions of complications and no comprehensive long-term follow-up of the patients that have been treated.²⁶ Reports from large databases lack granularity on these important issues. As such, the decision to use an endovascular approach for treatment of acute peripheral vascular injury should be made on an individual case-by-case basis.^14,16

Operative Management

The successful operative management of extremity vascular injuries requires prompt control of hemorrhage and timely restoration of adequate perfusion. These priorities must be orchestrated with the overall care of the patient. In the neurologically or hemodynamically unstable patient, other priorities will trump definitive vascular repair. In either case, damage control using a temporary intravascular shunt inserted into the appropriately prepared artery (and vein, if injured) can quickly restore perfusion in an ischemic limb,^27,28 while a tourniquet, appropriately applied (see below), can control hemorrhage.¹⁵ Secondary considerations include adequate tissue coverage of the vascular repair, fracture stabilization, and wound management.

Who Should Repair Injured Blood Vessel

Currently trauma surgeons with general surgery specialty training perform almost 70% of complex vascular repairs of injured arteries while vascular or cardiovascular surgeons perform 27% with similar rates of limb salvage (94% and 95%, respectively).²⁹ In an era of fewer open vascular procedures performed during general surgical training, the repair of extremity vascular injury in the future may not be within the capabilities of many trauma surgeons. It is important that senior trauma surgeons with experience in managing vascular injury train their younger colleagues in the techniques necessary to expose and repair these injuries. Because many surgeons who perform elective vascular surgery are not sufficiently experienced in the management of vascular trauma, board certification in vascular surgery does not qualify a surgeon as capable to handle these injuries just as the lack of certification does not necessarily disqualify a surgeon. Conversely, there are many trauma surgeons who are very skilled in vascular technique by virtue of their interest and experience. Surgeons with experience in vascular techniques and management of vascular injuries, no matter what the specialty training, should be available at all trauma centers.

Preoperative Preparation

Broad-spectrum antibiotics and, if there is a penetrating wound or open fracture, tetanus toxoid should be administered as soon as possible. If there is no evidence of ongoing bleeding in the limb and no intracranial or intracavitary hemorrhage, systemic unfractionated heparin should be administered (70 U/kg) as soon as possible after the diagnosis of ischemia is made.

In controlling hemorrhage there is no role for “blind” clamp placement in the injured extremity; it is rarely successful and frequently injures adjacent nerves. The operating room has the personnel and the equipment (including lighting and suction) necessary for effective exposure and control. A properly placed tourniquet, a Foley catheter with a 30-mL balloon inserted into the wound and inflated, or a gloved hand compressing the bleeding site during transfer to the operating room will suffice. There are a variety of commercially available disposable tourniquets that are very effective in providing temporary control. The tourniquet is placed proximal to the injury, but as distal as possible to avoid ischemia to tissues that are proximal to the injury. It should not be placed directly over joints or bony prominences as effectiveness may be reduced and the skin directly under the tourniquet will be at risk for ischemia by direct compression. Finally, it should be applied with pressure sufficient to occlude flow. The time of placement should be recorded to accurately track the occlusion time, which should not exceed 90 minutes to avoid nerve ischemia.¹⁵

If there is an associated fracture or dislocation, consultation with an orthopedic surgeon will facilitate preoperative planning. The sequence of procedures and conduct of the operation should be discussed, such as the use of a temporary vascular shunt to perfuse an ischemic extremity prior to orthopedic stabilization.¹⁶ Shunt placement and subsequent detection of Doppler signals in the limb distal to the shunt ensures perfusion and removes the sense of urgency to do a definitive repair. If there is extensive soft tissue loss, early consultation with a plastic surgeon will facilitate the planning of proper coverage of the vascular repair.

Once operative priorities have been established, communication with the operating room staff is necessary to ensure the availability of appropriate instrument sets, sutures and graft material, and other ancillary equipment, such as a cell saver for blood retrieval and a patient warming device. Communication with the anesthesiologist is necessary to inform them of the patient’s resuscitation needs, need for blood products, and estimated duration of the proposed operation.

The surgeon should be present in the operating room when the patient arrives to assist with specific operative preparation, which includes selecting suture and instrumentation appropriate to the proposed procedure,¹⁴ provision of heparinized saline (5000 U of heparin/500 mL) and papaverine hydrochloride (30 mg/mL) for regional injection. The surgeon should supervise positioning, prepping, and draping. To ensure that proximal control can always be obtained, areas of the adjacent chest and shoulder for upper extremity injuries and the adjacent abdomen (up to and including the umbilicus) for lower extremity injuries should be prepped and draped with the entire injured extremity.¹² Because the middle of the night is not the time to pull together the necessary equipment, it is prudent to assemble a standard “peripheral vascular trauma” set of equipment, sutures, and graft material ahead of time.

Principles of Operative Management

Exposure and Control

Proximal and distal control should be achieved prior to exposure of the vascular injury. The incisions for exposure are those used for elective procedures (see the section “Management of Vascular Injuries by Anatomic Region,” below). In proximal extremity injuries with active hemorrhage, the site is chosen to give the fastest exposure of inflow vessels for clamping. In mid and distal extremity vascular injuries where tourniquets have been applied to obtain control in the trauma resuscitation room, a sterile tourniquet can be placed. In the operating room, have one team member compress the bleeding site with a gloved hand and a sponge, remove the tourniquet, and prep the extremity. A 5000-U heparin bolus is then given if this is an isolated injury. The extremity is prepped and draped and a sterile tourniquet for use in the operating room (ie, one that contains a bladder for inflation and a gage for the measurement of cuff pressure) is placed proximal to the wound, inflated, and the pressure and time of inflation are documented. The injury site can then be explored in a controlled fashion and clamps or vessel loops placed above and below the vascular injury. The tourniquet can then be deflated.