Chapter 41: Peripheral Vascular Injury

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.

If, after proximal and distal control have been obtained, there is still ongoing hemorrhage from the wound area, an appropriately sized Fogarty balloon-tip catheter on a three-way stopcock can be gently inserted into the artery above or below the level of injury. The catheter is advanced to the area of the injury (measured beforehand against the Fogarty using the 10 cm markers on the catheter) and the balloon inflated enough to control the bleeding.

Control of proximal and distal flow is best achieved by “double passing” silastic vessel loops around the vessel above and below the area of injury and gently retracting until flow ceases. Side branches between the proximal and distal vessel loops are controlled with removable metal clips. If clamps are needed, choose the appropriately sized vascular clamp and close the ratcheted handle only as much as needed to occlude the vessel. Carefully support the clamps to avoid twisting and inadvertent stretching of the vessels.

Before initiating definitive repair of the injury, several sequential maneuvers are necessary. Inspect the injury and debride the injured parts back to normal appearing intima. Because flow has ceased with proximal and distal control, there may be proximal and distal thrombus in the vessel. Therefore, pass an appropriately sized Fogarty catheter proximally and distally to clear any thrombus. This must be done carefully because the intima can be injured by overdistention of the balloon; this is avoided by starting to retract the catheter before starting to inflate the balloon. When the slightest resistance or “drag” is appreciated stop inflating as the balloon is now in contact with the arterial wall. At this point continue with retraction of the catheter. Repeat catheter passes until no clot is retrieved from the proximal and distal artery. Inject heparinized saline into the proximal and distal artery using a vessel irrigator (Titus needle or olive tipped irrigator) first aspirating blood to insure that the tip is in the lumen. Care should be used flushing the proximal brachial artery and axillary artery because vigorous flushing of 10 mL may force thrombus or air into the origin of the vertebral arteries and cause a posterior circulation stroke.

The debrided and appropriately flushed artery should then be carefully inspected to select the method of repair that should be tension free. Normal arteries in the extremities of young patients are highly elastic and can retract a substantial distance. There is a significant risk of stenosis and thrombosis if undue tension is placed on the artery in an attempt to perform a primary repair of the distracted ends.

Transverse or short oblique lacerations without vessel wall disruption may be repaired with simple interrupted sutures. Longitudinal and long oblique lacerations cannot be closed without compromising luminal diameter. The injured site should be opened longitudinally for a length sufficient to inspect the intima. The injured or “questionable” intima should be debrided. A vein patch can then be used to close the arterial defect without compromising the diameter of the lumen. A polytetrafluoroethylene (PTFE) patch is an acceptable alternative in the common and superficial femoral arteries if vein is not available. If a long segment of the anterior arterial wall is debrided, leave the uninjured back wall intact. Leaving the back wall intact, rather than dividing it, prevents retraction of the arterial ends facilitating vein patch angioplasty or interposition grafting.

When there is complete vessel transaction, interposition grafting is usually necessary. The vessel ends should be “spatulated” or beveled to ensure a nonstenotic anastomosis. To ensure a tension-free anastomosis, mobilize proximal and distal segments of the normal artery even if it means sacrificing some minor tributaries. The optimal interposition graft material is autologous greater saphenous vein harvested from an uninjured leg. Native vein graft is preferable because it has elastic properties that make it very compliant with the normal pulsatile flow of an artery. It also has a diameter that approximates that of an extremity artery and produces an adequate size match for grafting in the arm and leg. Venous intima is less likely to be thrombogenic and it has superior long-term patency when compared with prosthetic material when used with smaller vessels (popliteal and tibial). When saphenous vein is unavailable, lesser saphenous vein should be used. Cephalic vein has been suggested as a suitable second choice, but cephalic vein is less muscular than the greater and lesser saphenous and will eventually dilate after it has been “arterialized.” Both the cephalic vein and the lesser saphenous vein are more difficult to harvest than the greater saphenous. If time of ischemia is a concern, one can insert a temporary shunt into the injured artery and vein and proceed with the harvest.

PTFE is an acceptable second choice. PTFE has a short-term patency of 70–90% and infections are rare even in contaminated wounds.³⁰ Patency of PTFE grafts is equivalent to that of vein for injuries proximal to the popliteal artery, but inferior to vein for popliteal and more distal vessels and that PTFE grafts of greater than 6 mm diameter should be used.³¹ All arterial repairs must be covered with soft tissue to prevent infection or desiccation of autogenous tissue, both of which can lead to hemorrhage or infection.

Single-vessel arterial injuries in the distal forearm and distal calf may be ligated if there is sufficient collateral flow through the remaining vessels. Observing back bleeding through the distal injured end of the vessel indicates adequate collateral flow. Doppler signals in the hand or forefoot vessels also indicate adequate distal perfusion. When in doubt, perform an intraoperative arteriogram.

Venous Repairs

Small veins can be ligated without sequela. Definitive repair of major veins (ie, femoral, superficial femoral, popliteal, axillary and subclavian) should be undertaken if the patient is physiologically stable; if unstable, utilize a damage control approach by inserting a temporary intravascular shunt into the appropriately prepared vein. The shunt should be placed in the distal end of the injured vein first to confirm proximal flow in the vein and to ensure that the shunt has not been placed in a valve cusp; the other end is then placed into the proximal vein and flow confirmed using Doppler interrogation. Lateral venorrhaphy, best performed with a running 6-0 or 7-0 Prolene suture, is possible in most venous injuries, taking care to avoid undue tension and “puckering” due to placing stitches too far apart and creating a purse-string effect. Vein patch closure or panel graft interposition is occasionally required. In the lower extremity, major venous ligation leads to venous hypertension in the calf and a higher risk for compartment syndrome. Autologous vein patch angioplasty should be considered in the more extensive injuries. The vein patch must be of a generous size to maintain adequate luminal diameter. Uncommonly, stab wounds result in a transversely oriented transaction that may be primarily repaired by simple anastomosis of the cut ends without causing significant stenosis. More extensive circumferential injuries require a saphenous vein panel graft interposition. This is performed by harvesting a long segment of saphenous vein, opening it longitudinally, wrapping it around a chest tube or other appropriate large cylindrical structure, and sewing it in a spiral fashion to create a panel graft. This large-diameter graft is a suitable conduit for venous reconstruction. This technique is tedious and requires significant vascular technical ability and experience. While preparing the panel graft, which is time consuming, a temporary shunt should be place into the severed ends of the vein (as described above). Postoperatively, a continuous passive motion device (as used in major orthopedic surgery) can be used to increase venous flow velocity, improve venous drainage, and prevent venous thrombosis following repair.³²

Intraoperative Assessment of Vascular Repairs

Technical problems occur in up to 10% of vascular repairs.³³ Therefore, objective assessment of the repair and the distal vascular bed must occur. Palpation of the distal pulses should be performed (another reason why the whole extremity is prepped) followed by a handheld Doppler interrogation of the repair and the vessel immediately distal to the repair. Constant high-pitched signals indicate stenosis and should prompt imaging. Intraoperative duplex scanning is useful but requires significant training and experience to perform and interpret the images. A completion arteriogram with either single-injection radiography or fluoroscopy is useful to detect platelet (“white”) thrombus at a suture line, kinking of an interposition graft, or an intimal flap, all of which may cause early failure.

Role of Tissue Coverage

Desiccation or superficial infection in the inadequately covered repair leads to suture disruption and hemorrhage. Therefore, all repairs must be covered with healthy tissue, preferably muscle. This is typically not a problem with simple stab wounds or gunshot wounds, but tissue avulsion from automobile or motorcycle crashes or debridement of devascularized tissue as a result of blast injury can compromise adequate coverage of a vascular repair. These often require rotation of regional muscle or local advancement of skin flaps. Early involvement of a plastic and reconstructive surgeon facilitates planning as a pedicled transposed muscle flap, free tissue transfer, myocutaneous flap, or fasciocutaneous flap may be indicated. However, complex myocutaneous flaps or free tissue transfer are inappropriate at the initial operation because they are time consuming and can put the patient at risk for hypothermia. These are more safely performed in a delayed fashion when the patient has recovered from the initial physiologic effects of injury. Vascular repairs can be temporarily covered by either cadaver skin graft or porcine xenograft.^34,35 The homograft or xenograft will be temporarily adherent, provide coverage, and often can stay in place for 5–7 days or longer. Subsequently, split-thickness skin grafting, tissue rotation, pedicle flaps, or free tissue transfer can be performed.

In extreme cases of tissue loss or subsequent disruption of an inadequately covered vascular repair, extra-anatomic bypass may be required. Preferably, an autologous vein bypass can be routed through adjacent healthy tissue in the extremity. Less commonly, externally supported PTFE grafts can be tunneled around the vascular injury site to supply distal perfusion as either definitive revascularization or as a temporizing step to allow healing and later placement of a vein graft through the site of injury.³⁶

Role of Fasciotomy

Unrecognized compartment syndrome following revascularization of an acutely ischemic limb is the most common cause of preventable limb loss following extremity trauma.¹² It must be remembered that compartment syndrome can be a manifestation of reperfusion injury (see the section “Pathophysiology,” earlier) and may not be immediately clinically apparent after revascularization. Thus, in patients with prolonged ischemia, closed fractures, crush injury, or combined arterial and venous injury, especially if major veins have been ligated, there is a role for “preemptive” fasciotomy in which fasciotomy is performed in conjunction with the initial vascular repair.^37,38,39 In those patients perceived to be a low risk for compartment syndrome (ie, knife wound with revascularization in <3 hours) compartment pressure should be measured routinely in the operating room before termination of the anesthetic. A commercially available device (Stryker Surgical, Kalamazoo, Michigan) facilitates initial and repeat pressure measurements (Fig. 41-4A). If not available, pressure tubing on a three-way stopcock with a blood pressure cuff and monometer may be used (Fig. 41-4B). There is no consensus regarding the exact pressure indicative of compartment syndrome; however, any pressure above 25 mm Hg should, at the very least, raise concern and suggest the need for repeated measurements and close observation for signs and symptoms of compartment syndrome (see the section “Complications and Outcome,” further).

Most trauma surgeons have experience with fasciotomy in the calf. Orthopedic surgeons more commonly perform fasciotomy in the upper arm, thigh, hand, foot, and buttocks.

Calf Fasciotomy

There are four compartments in the calf to release: anterior, lateral, and deep and superficial posterior (Fig. 41-5). The simplest release is performed using two long incisions (“double-incision fasciotomy”), one each on the lateral and medial aspects of the calf. Although isolated anterior compartment syndrome occurs rarely, it is recommended to release all four compartments.

The lateral incision should be generous; it begins 2 cm anterior to the fibula and 4 cm below the fibular head to avoid the peroneal nerve and is taken distally to within 2–3 cm of the lateral malleolus. The fascia of both the anterior and the lateral compartments can be released through this incision. It is critical to ensure that the anterior compartment is fully released by visualizing and palpating the tibia anteriorly beneath the incised fascia. Misplacing the skin incision posterior to the interosseous membrane can lead to mistaking the lateral compartment for the anterior compartment. This results in failing to release the anterior compartment. This failure can be avoided if the tibia is palpated medially through the releasing incision (beneath the opened fascia), as described above, and the intramuscular septum between the anterior and lateral compartment is palpated inferiorly beneath the open fascia of the anterior compartment.

The medial calf incision should be made 2–3 cm behind the posterior margin of the tibia to avoid lacerating the greater saphenous vein. The fascia over the gastrocnemius is fully released proximally and distally. In the distal calf, the gastrocnemius and soleus muscles are then retracted posteriorly to expose the deep posterior fascia. This layer is released carefully under direct vision to avoid lacerating the posterior tibial artery.

After the four compartments are released and hemostasis is obtained, a loose dressing is applied; tight dressings will recreate the syndrome when muscle swelling occurs. Postoperatively, the extremity should remain elevated to reduce edema formation and facilitate wound closure, which can occur in 48–72 hours. Split-thickness skin grafting may be required.

Thigh Fasciotomy

Thigh fasciotomy is uncommonly required. There are three compartments to release: lateral, medial, and posterior. Two generous incisions, one lateral for the lateral compartment and one medial for the other two compartments, are sufficient. If one is unfamiliar with thigh muscle anatomy, consult an orthopedic surgery colleague.

Forearm and Upper Arm Fasciotomy

Only those knowledgeable of arm and forearm anatomy and experienced in the procedure should perform fasciotomy in the upper limb. Orthopedic surgeons or hand surgeons are frequently consulted for assistance with the procedure. Generous dorsal and volar incisions release the dorsal and volar compartments and the mobile wad. Each major muscle group fascia must be individually incised. There are numerous superficial cutaneous nerves that must be carefully avoided. Upper arm fasciotomy is performed through medial and lateral incisions. There are medial and lateral muscle compartments to release and the deltoid compartment at the proximal extent of the lateral incision must also be addressed.

Vascular Damage Control

Vascular damage control is necessary when extremity vascular injury is associated with major torso injuries in an unstable patient. It involves rapid control of hemorrhage and prompt restoration of blood flow with temporary intraluminal shunts.^27,28,40 Fasciotomy may be part of damage control in the high-risk patient (see the section “Role of Fasciotomy,” earlier).

Ligation should be reserved for those arteries with adequate collateral flow. For example, in the upper extremity, injuries to either the distal radial or ulnar arteries may be treated by ligation provided there is evidence of adequate distal collateral flow assessed by either physical examination or continuous-wave Doppler interrogation. Similarly, in the lower extremity, ligation of a single tibial vessel or the peroneal can be performed following a similar assessment. If there is doubt about the adequacy of collateral circulation (ie, the patient is in profound shock) insert a temporary intraluminal shunt. Ligation of the brachial, external iliac, and superficial femoral or popliteal arteries has a high likelihood of producing limb-threatening ischemia resulting in amputation and should be avoided.

There are a variety of commercially available shunts that can be used for damage control. The 10 or 12 French straight carotid shunts are the most commonly used for this purpose. If these are not available, sterile intravenous tubing or endotracheal suction tubing of adequate size can be used to shunt both the artery and the vein of the extremities. Venous shunt placement instead of ligation may improve extremity perfusion and lower the risk of compartment syndrome. The common femoral vein may be shunted with a pediatric chest tube.

Damage control shunt placement begins with obtaining adequate proximal and distal control. Thrombus should be cleared, as previously described, followed by the instillation of regional heparinized saline (10 U/mL). The shunt should be placed in a straight line and long enough to remain safely held in place in the proximal and distal vessel with secured umbilical tapes or 2-0 silk ties. Long, looped shunts run the risk of becoming dislodged during subsequent dressing changes and should be avoided. If a patient is to be transferred to another facility, place a tie around the center of the shunt with one end of the ligature tied to the proximal and one end tied to the distal shunt ligatures that are securing the shunt in the vessel. This will ensure that the shunt is not dislodged during the transport. Securing the shunt with ligatures necessarily injures the intima at the site of their placement; those portions of the artery must be debrided at the time of definitive vascular repair.

If there is injury to a major proximal vein of the lower extremity, it should not be ligated but should be shunted (as described earlier, see the section “Venous Repairs”). This allows the option of repair versus ligation at a time when the patient is stable. Ligation will result in venous thrombosis and subsequent venous repair will not be possible. However, in dire situations with a profoundly unstable patient, venous ligation may be the best option. After major lower extremity venous ligation consider calf fasciotomy to forestall the development of compartment syndrome.

The timing of definitive vascular repair following damage control procedures is determined by condition of the patient. Hemorrhage must be controlled and hypothermia, coagulopathy, and acidosis must be corrected prior to returning the patient to the operating room. Concern for shunt patency should not drive the decision to return to the operating room. The patency of temporary shunts used for damage control is 95%, even with protracted “dwell times” of up to 72 hours.^27,28

Combined Arterial and Skeletal Extremity Trauma

Vascular injury complicates less than 2% of extremity fractures and dislocations, but skeletal trauma is present in 10–70% of patients with extremity vascular injuries.⁴¹ In both civilian and military series, combined arterial and skeletal extremity trauma carries a substantially higher risk of limb loss than does isolated skeletal or isolated arterial injury.^42,43

Successful management requires both prompt diagnosis and coordination of the efforts of both the orthopedic and vascular surgeon. Treatment priorities must be discussed, that is, should fracture fixation go before repair of arterial and venous injuries. Each case must be individualized, but concern regarding the priority of either definitively reestablishing blood flow to an ischemic limb or fixating the fracture as the first priority is allayed by inserting a temporary intraluminal shunt. This can be done relatively quickly and the orthopedic surgeon may then proceed with fracture fixation. Once the extremity is stabilized, the definitive vascular repair can be performed. Combined injury damage control in hemodynamically or neurological unstable patients consists of placement of intravascular shunts, fasciotomy, and external fixation.

The Mangled Extremity

The ultimate in combination injuries of the extremity has been euphemistically termed “mangled” because it consists of severe injury to the bones, muscles, soft tissues, nerves and vessels as a result of high-energy transfer. The amputation rate for mangled extremities remains at 20%.⁴⁴

The grotesque appearance of these threatened limbs can be a distraction from the more severe associated injuries of the head and torso. Focus must be shifted to the initial evaluation or primary survey using ATLS guidelines (see the section “Clinical Presentation,” earlier). Hemorrhage from a mangled distal extremity can be controlled with proximal tourniquet application (see the section “Preoperative Preparation,” earlier). If extremity hemorrhage cannot be controlled or the patient is persistently hypotensive, proceed to the operating room where cavitary injuries can be addressed and the instrumentation and ancillary equipment necessary for extremity management are available.⁴⁵ The complexity of this type of injury mandates collaborative evaluation with orthopedic, neurosurgical, and plastic and reconstructive surgery consultants to address management options—one of which is amputation. If skin and soft tissues are the only attachment of the mangled limb to the torso, immediate amputation is indicated.⁴⁵ A management algorithm based on the existing literature and expert opinion recommends the following general principles in the stable patient: restore anatomic alignment of fractures, perform vascular and neurologic assessments (see the section “Diagnostic Evaluation,” earlier), obtain multispecialty consultation with regard to individual injury components (ie, bone, nerve, and soft tissue) in the operating room and overseen by the trauma surgeon, and make a collaborative decision to attempt salvage or amputate based on that assessment.⁴⁵ If a decision cannot be made, damage control procedures should be undertaken and a planned return to the operating room in 24 hours is scheduled. Photographs and extensive notes articulating the nature of injuries and the decision-making process are recommended at the end of the initial procedure. These are helpful for comparisons at the second operation and are useful for accurate communication with the patient and the family in the interim. The use of scoring systems to reliably predict the need for amputation has not been useful because the limb salvage rate has been consistently higher than predicted.^46,47,48

Early Postoperative Management

Technical problems with the vascular repair are most likely to present within the first 24 hours postoperatively. Therefore, close clinical surveillance is essential and includes repeated pulse examination and frequent assessment of the extremity for compartment syndrome (see the section “Compartment Syndrome,” further). The onset of new neurologic deficits is an important indicator of continuing ischemia and should prompt assessment of the patency of the vascular repair and the pressure within muscular compartments. Loss of a palpable pulse, pallor replacing rubor (following ischemia the re-perfused limb should be hyperemic after re-warming), and a loss of or a change in the character of the Doppler signal (monophasic replaces triphasic or biphasic) should prompt a return to the operating room.

The use of anticoagulation and antiplatelet medications in the early postoperative period is discouraged in patients with multiple injuries secondary to blunt trauma. Full anticoagulation with heparin is reserved for isolated penetrating extremity injuries with repair of small vessels.

Management of Vascular Injuries by Anatomic Region

The following sections provide information regarding the management of injuries to specific arteries based on their anatomic location. It is assumed that the recommendations for diagnosis and management described above are utilized since they are applicable to all regions.

Upper Extremity

Because of their proximity to the nerves of the upper extremity, vascular injury is frequently associated with an injury to the adjacent nerve. When combined injuries do occur, the nerve injury, rather than the vascular injury, determines the quality of the outcome.^49,50 Compared to the lower extremity, the arteries of the upper extremity are less muscular, which means they must be handled with extreme care during operative repair.

Subclavian and Axillary Vascular Injuries

Subclavian injuries are the least frequent of extremity vascular injuries. The most common mechanism of injury is penetrating to either the chest, base of the neck or shoulder; 50% of patients with a subclavian injury will be in shock. Blunt mechanisms produce contusions with intramural hematoma, laceration from shards of a fractured first rib or clavicle, or intimal disruption with thrombosis. A chest radiograph with radiopaque markers placed over any penetrating wound(s) is essential. A hemothorax, an apical cap, or an elevated hemidiaphragm (as a result of phrenic nerve injury) should arouse suspicion of a subclavian injury.

Exposure requires a wide prepping and draping of the ipsilateral shoulder, lower neck, chest, and arm. Proximal control on the left may require an anterolateral thoracotomy through the third intercostal space. On the right, sternotomy may be required for proximal control. Distal control may require an infraclavicular incision. The site of injury is then approached directly through a supraclavicular incision. The right subclavian is more easily approached than the left because it rises higher relative to the clavicle. An effective adjunct to proximal control in the case of a partial arterial wall laceration is the introduction of a balloon-tipped catheter retrograde through the axillary artery to the site of injury. The subclavian may then be directly approached. Surgical exposure can be difficult because of the clinically important structures closely allied with the subclavian.¹² Division of the anterior scalene should only be done after the phrenic nerve has been identified (going medial to lateral across the belly of the anterior scalene) and mobilized (carefully). If the clavicle is obstructing either the exposure or the repair, it can be divided or completely removed without sequela.⁵¹ The subclavian artery has a thin muscular coat and it is very intolerant of heavy-handed traction, imprecise suturing or excessive tension. The third portion of the subclavian artery (between the lateral border of the anterior scalene and the lateral border of the first rib may be exposed by dividing the clavicle at the junction of the proximal third with the distal two-thirds and retracting it inferiorly to be reattached later, or completely removed.

Exposure of the axillary vessels is obtained through a transverse infraclavicular incision carried down to the pectoralis minor muscle by splitting the fibers of the pectoralis major muscle. The pectoralis minor tendon is divided at its insertion on the coracoid process; it will then retract out of the way. The axillary artery and vein are located immediately below the muscle (Fig. 41-6). Care must be taken to avoid the cords of the brachial plexus, which are in close proximity to the axillary vessels. More distal exposure may require completely dividing the pectoralis muscle; however, this is uncommonly needed.

Injuries of the subclavian and axillary vessels are rarely amenable to simple suture repair. Subclavian and axillary arterial injuries are preferentially repaired with an interposition of externally supported (“ringed”) PTFE. Venous injuries may be ligated unless there is extensive soft tissue injury with disruption of collaterals. Occasionally, vein or PTFE patch repair is possible. The risk of venous hypertension is low and ligation should be used unless the vein repair can be done expeditiously. Forearm or upper arm fasciotomy is rarely required with vascular injuries at the subclavian and axillary level. However, close follow-up in the postoperative period for the development of compartment syndrome is mandatory.

Severe blunt trauma to the shoulder and upper extremity can cause complete disruption of the musculoskeletal support of the shoulder girdle producing what has been termed “scapulothoracic dissociation” or a “closed” forequarter amputation. A common mechanism is high-speed motorcycle crash. The diagnosis can be made from a chest radiograph that shows ipsilateral sternoclavicular dislocation and lateral displacement of the medial border of the scapula (Fig. 41-7). The brachial plexus and either the subclavian or axillary artery and vein can be completely disputed or severely stretched producing a large hematoma and a pulseless, flaccid, and insensate upper extremity. The outcome is uniformly poor because of the neurologic injury.^49,52 Because of the abundant collateral circulation around the shoulder, the loss of the pulse with scapulothoracic dislocation is rarely associated with limb-threatening ischemia. It may even be necessary to ligate the subclavian artery to obtain hemostasis. Recent publications have confirmed the observations of Rich and Spencer⁵³ that the subclavian artery can be ligated without producing ischemia and that loss of a radial pulse following scapulothoracic dissociation has minimal risk of ischemia.^52,54 Many patients ultimately request amputation because of the burden of an insensate and paralyzed arm that sustains repeated injury.

Endovascular management has been increasingly reported for axillary and subclavian injuries.^24,55 The apparent and theoretical advantages of endoluminal management include reduced morbidity and blood loss.⁵⁵ However, a recent meta-analysis showed a lack of superiority of endovascular management over open treatment (pooled mortality rate for open: 12.4%; pooled mortality for endovascular: 26%), but the evidence remains weak due to extreme heterogeneity among patients treated and significant publication bias.²⁶

Brachial Artery Injuries

Brachial artery trauma is most frequently penetrating from interpersonal violence or laceration from glass shards. Supracondylar humerus fracture is the most commonly associated orthopedic injury.

Prepping and draping for proximal or distal injuries should include the shoulder and infraclavicular region as well as the entire arm to the fingertips; the distal arm can be draped with a sterile sleeve, which can be rolled up or cut for additional exposure or to palpate the radial pulse.

Exposure is obtained through a longitudinal incision over the course of the artery on the medial aspect of the upper arm. Proximal control for high brachial artery injuries may require control of the axillary artery in the infraclavicular region. Distally, the incision can be extended with an S-shaped extension across the antecubital fossa from ulnar to radial aspect and onto the forearm to expose the origins of the forearm vessels.¹²

Proximal control for injuries of the distal brachial artery and the forearm vessels may be temporarily obtained with a sterile pneumatic tourniquet. This adjunct, however, should be removed as soon as vessel loops or vascular clamps can be applied in order to restore collateral flow.

Simple lacerations may be treated by direct suture repair if the repair can be performed without tension. Saphenous vein interposition should be chosen whenever vessel injury is extensive or if primary tension-free repair is not possible. There is no role for brachial vein repair unless there is extensive soft tissue injury.

Forearm fasciotomy, particularly in the setting of prolonged ischemia, must always be considered prior at the completion of the brachial artery repair. Intraoperative compartment pressure measurements may be normal, but reperfusion edema and swelling can produce a delayed compartment syndrome. Repeated postoperative follow-up is essential to identify this delayed complication.

Forearm Arterial Injuries

The brachial artery gives rise to the ulnar and radial arteries after crossing the antecubital fossa. The ulnar artery is larger than the radial artery in the upper arm and gives rise to the interosseous artery. Although the radial artery is more superficial and easily palpated at the wrist, the ulnar artery is the dominant blood supply to the hand in 60% of patients. Both vessels contribute to the superficial and deep palmar arches. The ulnar artery is the dominant supply to the palmar aspect of the hand and the radial artery is the dominant supply to the dorsum. The palmar arches are incomplete in up to 30% of patients.

Prepping and draping should include the hand, wrist and arm to the axilla. Exposure is obtained through a longitudinal incision on the volar aspect of the forearm, taking care to avoid the many cutaneous nerves in this area.

Combined ulnar and radial artery injuries in the forearm require repair of at least one vessel. The ulnar artery is usually larger in the proximal forearm and is a better target for saphenous vein bypass. Distally, repair should be performed in whichever vessel is larger or less injured and more amenable to simple repair. Collateral flow should be evaluated by either completion arteriogram or Doppler interrogation, which should include the palmar arch and proper digital arteries.

Isolated ulnar or radial artery injuries can be ligated if there is absolute certainty that flow through the remaining vessel is adequate. Close inspection of the forearm and hand with palpation of pulses augmented by Doppler interrogation is essential. Isolated forearm arterial injury may be repaired if the patient is stable and there are no other pressing management priorities.

Lower Extremity Vascular Injuries

Lower extremity vascular injuries are most commonly caused by penetrating injury. Supracondylar fractures of the femur or dislocation of the knee should be viewed with a high index of suspicion for an arterial injury. There is a role for liberal use of prophylactic compartment release following lower extremity vascular injuries when there has been prolonged ischemia.

Common Femoral Vascular Injuries

Prepping and draping should include the foot and the ipsilateral lower quadrant of the abdomen; this allows exposure of the external iliac for proximal control, if necessary (Fig. 41-8). A longitudinal incision over the common femoral vessels should be generous enough to expose the bifurcation so that both the superficial femoral and profunda femoris arteries can be controlled with encircling double-passed silastic vessel loops. Primary repair is occasionally possible, but most injuries are complex and require either a saphenous vein or PTFE interposition graft.

Femoral vein injuries are also more often complex. They usually require careful clamp placement for vascular control. There are numerous side branches that must be controlled. Vein clamping results in venous hypertension if the artery is not also occluded. Vein patch repair, saphenous vein panel interposition, or heparin bonded, externally supported PTFE may be required. In unstable patients, venous ligation may be the best course of action. However, if there is sufficient time, shunting of the common femoral vein using a pediatric chest tube may the prevent venous hypertension associated with ligation and, with maintenance of femoral venous return, may augment cardiac filling. Calf fasciotomy should always be considered when the major veins of the lower extremity are ligated.

The profunda femoral artery is well collateralized by branches of the hypogastric (internal iliac) artery.¹² Although simple lacerations should be repaired, more extensive injuries should be ligated unless there is extensive soft tissue injury and loss of collaterals in the buttock and upper thigh. However, a preexisting stenosis or occlusion of the superficial femoral artery necessitates repair of the profunda femoral artery because of its important role in providing collateral flow to the leg.

Superficial Femoral Vascular Injuries

Prepping and draping is similar to that presented for common femoral artery injuries. Exposure of the proximal superficial femoral is obtained through a longitudinal groin incision previously described. The mid-portion is located just behind sartorius muscle as it travels from superior lateral to inferior medial in the thigh.¹² The sartorius muscle is retracted either anteriorly or posteriorly to expose the superficial femoral artery and vein. The incision should be long enough to obtain both proximal and distal control. Although simple repair may be possible in some wounds, most require an interposition graft. Reversed autologous saphenous vein from the uninjured leg should be used if at all possible. The superficial femoral vein should be repaired, if possible. Consideration should always be given to calf fasciotomy in any patient with superficial femoral arterial injury with prolonged occlusion and those with ligation of the superficial femoral vein. If fasciotomy is not performed, compartment pressures should be measured both before leaving the operating room and frequently in the early postoperative period.

Popliteal and Tibial Artery Injuries

The popliteal artery is fixed in position at the adductor tendon proximally, the geniculate collaterals at its mid-portion, and the gastrocnemius distally. These points of fixation at the knee joint place it at risk for injury when the knee is dislocated. In full knee extension, the popliteal artery is under considerable tension. In hyperextension even more so—as the back of the tibial plateau moves posteriorly in a dislocation, it impacts and stretches the popliteal artery, often completely disrupting it. The popliteal vein may suffer the same fate. Because the amputation rate remains 20–30% following a posterior dislocation of the knee^12,43 and because the pulse examination may be insensitive,⁵⁶ a CTA with 3D reconstructions is reasonable for this injury.

With the patient in the supine position, prepping and draping is done from the groin to the toes. Adequate exposure requires a medial incision from the proximal popliteal space to the distal popliteal space with care not to injure the greater saphenous vein.¹² Division of the medial head of the gastrocnemius muscle and the semimembranosus and semitendinosus tendons provides a complete view of the popliteal artery and vein and the tibial nerve. This ensures adequate vascular control and the opportunity for successful repair. When closing the wound, approximation of the divided gastrocnemius muscle and semimembranosus and semitendinosus tendons with absorbable sutures will ensure an excellent functional result. Distal popliteal and proximal tibial vessel injuries are approached through a medial incision below the knee along the posterior margin of the tibia. This may be extended distally by dividing the soleus muscle over the course of the tibial-peroneal trunk and the posterior tibial vessels.

Popliteal and tibial artery injuries are usually complex and primary repair is rarely possible. Saphenous vein interposition is the best method of reconstruction. PTFE should be avoided because it has a high late failure rate when crossing the knee joint.

Empiric four-compartment calf fasciotomy should be considered when the interval of ischemia exceeds 3–4 hours. It should always be performed in the setting of combined popliteal arterial and venous injuries.

Tibial vessel injuries may be ligated if there is adequate flow through the remaining vessels. When in doubt, an intraoperative arteriogram or Doppler interrogation of the dorsalis pedis and posterior tibial arteries in the foot should be obtained. In multiple tibial vessel injuries, a saphenous vein interposition should be performed to the distal tibial vessel that best supplies the foot and that can be most easily covered with healthy soft tissue.

Complications following surgery for a vascular injury are those that are generic to any operation, such as a surgical site infection, and those that are parochial to the vascular repair, such as graft thrombosis, and those that may be a combination of the two, such as amputation. Each of the major complications will be discussed in that context

Surgical site infection

The surgical site infection rate following interventions for extremity vascular trauma is not often reported, but some generalizations can be made. It is more common after blunt injury; of the penetrating mechanisms, it is most common after explosive injuries and shotgun wounds, both of which produce significant soft tissue trauma, moderate local contamination, and interruption of the local blood supply to the skin and subcutaneous tissue.

Preventative measures are best practice. These include preoperative broad spectrum antibiotics with intraoperative scheduled re-dosing particularly when the procedure is long (ie, combined with an orthopedic procedure), and the blood loss is substantial. Preemptive debridement of nonviable and potentially nonviable skin and soft tissue at the initial operation is paramount. This can be followed by pulsed irrigation containing either antibiotic solution or saline.⁵⁷ For severe injuries (see the section “Mangled Extremity,” earlier), scheduled return(s) to the operating room for examination under anesthesia provide an opportunity to perform additional debridement and to assess viability of local tissues.

A surgical site infection that extends to a vascular graft or to the site of a vascular repair or anastomosis can lead to graft thrombosis or exsanguinating hemorrhage. Infection of a vascular suture line may present as a “herald bleed”—a small amount of hemorrhage from a wound considered to be stable and healing. The “herald bleed” abates only to be followed later with significant blood loss. Wound dehiscence or wound infection with even remote suspicion of a graft infection merits examination under anesthesia in the operating room. If the graft is not exposed and the deep layers of the wounds appear uninfected, proceed with culture of the wound, aggressive debridement of the superficial layers, wound irrigation, and packing of the open wound. After the first or second dressing change vacuum assisted closure can be used. In complicated wounds, a muscle flap to cover the vascular repair site is the best way to avoid infection and vessel erosion with hemorrhage. Once a repair has eroded and bled, it should be debrided back to healthy-appearing artery, ligated, the stump covered with viable tissue, and the graft replaced with an extra-anatomic bypass.³⁶

Amputation

Amputation remains the most significant of the complications following extremity vascular trauma. As has been pointed out previously, amputations of the upper extremity are less frequent, most likely because of the extensive collateral circulation around the shoulder.¹³ Factors associated with limb amputation are blunt mechanism, time to reperfusion of an ischemic limb, protracted hypovolemic shock, extensive soft tissue injury (see the section “Mangled Extremity,” earlier), popliteal artery injury, failed revascularization, and unrecognized and untreated compartment syndrome (see the section “Compartment Syndrome,” further). Technical failures, such as a narrowed anastomosis or a twisted graft (see the section “Technical Problems,” further), can lead to amputation, but these are not common, particularly if intraoperative completion arteriography is performed (see the section “Intraoperative Assessment of Vascular Repairs,” earlier).

Amputation rates during the index hospitalization can vary from 5% to 20%; higher rates are reported from military conflicts with massively destroyed limbs undergoing early amputation in theater, while lower rates are reported from civilian centers with mostly isolated penetrating trauma.^29,58 Long-term follow-up of patients with vascular injury is sparse, but the void is now being addressed with a concurrent multicenter study.⁵⁹ The late amputation rate due to severe nerve injury producing chronic pain and allodynia is unknown.

Missile Emboli

Intravascular migration of bullets, shotgun pellets, and other foreign bodies is uncommon and occurs in less than 1% of extremity vascular injuries.⁶⁰ The most common occurrence is the migration of small-caliber shotgun pellets from the proximal extremity veins through the right side of the heart and into the pulmonary circulation. Larger bullets may enter arteries and embolize to distal vessels causing ischemia. Bullets that enter the great veins may embolize proximally to the heart or, by the force of gravity, travel in a retrograde fashion into the lower extremity veins.

Diagnosis requires a high index of suspicion and a thorough peripheral vascular examination. Entrance wounds without associated fragments, pellets or bullets on radiographs of the injured limb should raise the alert that “missile” embolism may have occurred. Arterial obstruction by an offending missile embolus producing acute limb ischemia requires prompt operation for bullet retrieval. In the absence of limb threat, angiography and snare deployment under fluoroscopy can be successful for missile retrieval. A cut down under local anesthesia at the snare introduction site is usually required to remove the retrieved bullet. Asymptomatic small-caliber shotgun pellets in the extremities are best left alone.

Compartment Syndrome

All muscle compartments in the extremities are vulnerable to intra-compartmental hypertension that can eventually produce a “compartment syndrome” leading to nerve and muscle necrosis. A compartment syndrome can be caused by hemorrhage from direct trauma or reperfusion following ischemia (see the section “Pathophysiology,” earlier). Compartment syndrome results from swelling of muscle in a confined space (ie, bound by rigid structures such as fascia and bone). This swelling increases the tissue pressure within the confined space or “compartment” compressing both venous and lymphatic outflow and, eventually, arteriolar inflow, further increasing tissue pressure and reducing perfusion, ultimately resulting in ischemic neuropathy and myonecrosis if not treated promptly. Compartment syndrome occurs most commonly in the muscle compartments of the lower leg. It may be life threatening because of the systemic effect of rhabdomyolysis with subsequent myoglobin-induced renal failure and hyperkalemia.

The anterior compartment is the most vulnerable. Acute complete traumatic occlusion or ligation of the popliteal vein will increase tissue pressure enough to cause compartment syndrome, particularly in the anterior compartment. The upper extremity has more extensive venous drainage and is less prone to develop compartment syndrome than the lower extremity following venous occlusion or ligation. Compartment syndrome follows less than 10% of brachial artery injuries and is not a complication of upper extremity venous ligation unless there is extensive soft tissue injury.⁶¹

Technical Problems

Despite meticulous techniques, some grafts fail. They fail because of problems with the inflow, the conduit, or the outflow. Intraoperative completion angiography will detect most conduit problems (ie, kinking or a 360° twist of a tunneled vein), but may miss inflow and outflow problems. For this reason, compulsive repeat examinations of the blood pressure and the runoff bed are mandatory. A patient who had a palpable distal pulse in the cold operating room, but has no palpable pulse in the warm recovery room should raise concern for a technical problem. In this case, check the patient’s blood pressure; if the patient is hypotensive and has lost the pulse in the contralateral extremity the issue is inflow and is systemic and not local. Proceed with resuscitation and investigation of the cause of hypotension. If the contralateral pulse returns with resuscitation, but the ipsilateral does not the problem is local and the patient should be returned to the operating room. If the patient did not have a pulse in the cold operating room and had a satisfactory completion arteriogram and biphasic continuous wave Doppler signals in the runoff bed, use the Doppler and physical examination to follow the distal circulation. Often a palpable pulse will return and the previously ischemic runoff bed will be hyperemic in the normothermic patient. Postoperative vascular checks must be performed frequently. If there is any doubt about patency, the patient should be returned to the operating room for direct inspection of the repair. If there is no pulse in the graft or distal artery, catheter thrombectomy followed by completion angiography is necessary.

The most common causes of early failure are technical errors. These include intimal flaps, kinking, undue tension, and stenosis at the site of repair or anastomosis. Less commonly, platelet thrombus accumulates on a technically adequate repair. This may occur from the generalized platelet activation of injury. It is often associated with extensive muscle or crush injury. Less commonly it is a manifestation of a heparin allergic reaction and activation in the process of heparin-induced thrombocytopenia. Low-molecular-weight dextran (40,000) should be given as a 40-mL bolus and then infused at 40 mL/h for 24 hours. Once the repair has been reopened by thrombectomy, it should be followed closely for recurrent occlusion and heparin-induced thrombocytopenia should be investigated.

Postoperative anticoagulation is not usually helpful in arterial repairs for vascular trauma. However, it may have a role in venous repairs and should be considered in otherwise stable patients.⁶²

Post-Traumatic Pain Syndromes

The ultimate outcome from extremity vascular injury is largely determined by the associated musculoskeletal and neurologic injuries. The neuropathic or insensate extremity will severely limit functional capacity, not only of the limb, but also of the patient. Complex Regional Pain Syndromes (I and II, previously termed reflex sympathetic dystrophy and causalgia, respectively) are disabling neuropathic syndromes that can occur following mild to severe injury. The pathophysiology is poorly understood.⁶³ Patients may complain of hyperalgesia or allodynia that may become so severe that they will not touch or move the limb. If the diagnosis is suspected a diagnostic sympathetic block should be performed. If successful (moderate to complete relief of pain), the patient should be offered a sympathectomy. The earlier this is done in the course of the disease the more likely sympathectomy will produce long-term benefit.

Ambulatory Venous Hypertension

Late sequelae from venous injuries can be more troublesome than those of arterial injuries. Thrombosis following venous repair is not uncommon, but the vein will usually recanalize, the process of which can lead to valvular dysfunction, venous insufficiency, and ambulatory venous hypertension. If untreated, postphlebitic syndrome occurs, which can be disabling. Compressive support stockings should be given to all patients following venous repair. Because patient compliance with wearing support hose is very poor, patient education is critical in gaining their cooperation.

Pseudoaneurysm and Arteriovenous fistula

Late development of either a pseudoaneurysm or an arteriovenous fistula is very uncommon due to improved modalities of diagnosis of arterial injury in the acute phase of care. These complications may occasionally be missed or may become apparent weeks to months after injury. For these reasons, patients who have had complex vascular repairs should be followed with duplex ultrasound on a yearly basis. Arteriovenous fistulae and pseudoaneurysms are amenable to either open or endovascular treatment.