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Management of Civilian and Military Vascular Trauma: Lessons Learned
Management of Civilian and Military Vascular Trauma: Lessons Learned Tony Nguyen, MD, Jeffrey Kalish, MD, and Jonathan Woodson, MD Management of vascular trauma has evolved tremendously since the turn of the 20th century. The lessons from each major military conflict over the past 100 years have refined our understanding of how to care for soldiers and civilians with vascular injuries. The recent wars in Iraq and Afghanistan have likewise improved our strategy for treating victims of vascular trauma. Understanding the principles that guide management of vascular injuries will result in preservation of life and limb. Semin Vasc Surg 23:235-242 © 2011 Elsevier Inc. All rights reserved.
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IPPOCRATES IS CREDITED with saying, “he who wishes to be a surgeon should go to war,” and its truth is evident in the origins and development of current vascular surgical trauma care. Wars have always produced large numbers of sick and wounded, which challenged physicians to improve the practice of medicine and surgery through development of new procedures, therapies, systems, and paradigms for care. Boiling oil and cautery of ancient wars gave way to arterial ligation. Better sanitation and shorter, improved evacuation systems allowed the appropriate conditions to develop techniques to repair arteries. Ligation of injured vessels was still the predominant method of handling vascular trauma through the end of World War II. Arterial repairs and vein bypass grafting, resulting in a decrease in amputation rates (50% to 13%) and greater advances in limb salvage, arrived with the advent of mobile surgical hospitals and vascular specialty centers from the Korean and Vietnam Wars. Through the Vietnam Vascular Registry, a large volume of data was collected and analyzed, which led to development of best practices in the management of vascular trauma. The military lessons were disseminated to and further refined in the civilian sector.1,2 Modern-day civilian trauma algorithms are rooted in the lessons learned on the many battlefields across the world.
Epidemiology Trauma remains the leading cause of death in the 15- to 44-year-old age group in the United States, as a consequence
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0895-7967/$-see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1053/j.semvascsurg.2010.11.004
of unintentional injury, assault, homicide, and suicide.3 The distribution of civilian vascular trauma has not changed much throughout the decades; penetrating trauma is still the predominant etiology (70% to 80%), while blunt trauma constitutes 5% to 15% of injuries. Of the penetrating injuries, most (50% to 80%) are sustained from gunshot wounds, and stab wounds are less prevalent (10% to 30%). In addition, iatrogenic vascular injury has been increasing in prevalence as the number of invasive procedures increases. In fact, it has been described as high as 33% of all vascular trauma at a Level I trauma center.4 Overall, arteries are more often injured than veins, and extremities are injured more than other anatomical regions (similar to reported military experiences).5
Pathophysiology Successful management and treatment of vascular injuries requires an understanding of the pathophysiology and biomechanics of vascular trauma. On a simplistic level, vascular trauma is categorized into two types: blunt or penetrating. However, the severity of injury is a consequence of multiple factors: (1) direct injury to vessels from missiles or penetrating objects; (2) the transfer of energy and heat to tissues (kinetic energy). This results in cavitation effect (shock wave) of high-velocity moving objects as it penetrates tissues and will cause a zone of injury at a distance from the path of the missile tract; (3) the shearing or compressive forces of rapid deceleration in the case of blunt trauma. This can lead to contusion, tearing, thrombosis, intimal flap, and dissection of blood vessels; and (4), although uncommon, the embolization of foreign objects (fragments, shotgun pellets, or bullets), which can potentially cause distal vessel injury, occlusion, or thrombosis. 235
T. Nguyen, J. Kalish, and J. Woodson
236
Basic Principles of Open Management of Vascular Trauma Management of vascular trauma begins with the initial triage, evaluation, and resuscitation of the trauma patient. Appropriate attention must be paid to the airway, ventilation, and external hemorrhage control, and circulating blood volume should be restored. Immediate hemorrhage control can often be obtained by direct pressure or application of tourniquets on extremities. Once hemorrhage is controlled, then resuscitation is continued through the remaining primary and secondary survey in accordance with Advanced Trauma Life Support protocols to identify and prioritize all associated injuries. The patient with multiple injuries needs detailed assessment before embarking on complex or lengthy vascular repairs. Unrecognized severe intraabdominal or intracranial injuries can lead to disastrous outcomes if not addressed early. Pericardial effusions and cardiac contusions can render the patient too unstable to proceed with complex repairs. Vascular shunts have been used with increasing frequency to permit temporary reperfusion of extremities while other injuries are treated. Diagnosing vascular injury without any obvious source of external hemorrhage is more challenging. Signs and symptoms of arterial injury can be described as “hard” and “soft” (Table 1). Hard signs, such as active arterial hemorrhage, expanding hematoma, loss of distal pulse, signs of ischemia, and a bruit or thrill are highly suggestive of arterial injury. Profound signs of ischemia include the classic 6 “Ps”: paresthesia, paralysis, pulselessness, pain, pallor, and poikilothermia. With such findings, no diagnostic imaging is usually required before surgical exploration of extremity vessels. Soft signs raise the suspicion of arterial injury and include moderate-sized hematoma, history of significant blood loss or hypotension at the prehospital scene, proximity of wound to vascular structures or bony injuries, diminished distal pulses, and ipsilateral neurologic deficits. Soft signs can warrant additional diagnostic imaging, duplex studies or observation with repeated interval physical examination. Ankle-brachial index (ABI) is an objective bedside diagnostic procedure that is instrumental in the management of lower-extremity trauma patient. An ABI of ⬍0.9 may suggest arterial injury and need for further diagnostic imaging.6 A
Table 1 Clinical Signs of Arterial Injury: Hard Signs Warrant Surgical Exploration and Control, Soft Signs Afford Time for Further Diagnostic Imaging Hard
Soft
Arterial bleeding Loss of pulse Expanding hematoma Bruit or thrill
History of prehospital blood loss Diminished pulse Moderate hematoma Proximity to large vessel or bony injury Signs of ischemia (6 Ps*) Ipsilateral neurologic deficit *Paresthesia, paralysis, pulselessness, pain, pallor, and poikilothermia.
good history and examination of the uninjured contralateral limb is important for interpreting ABIs. Older patients with peripheral vascular disease may present with reduced ABIs, confusing the issue. Once the decision for operative repair has been made, the basic principles for management of vascular trauma apply irrespective of types and location of injury. Before exploring the injured vessel, proximal and distal control must be obtained. This is especially important in injuries that have ceased bleeding due to an adherent clot or if the offending penetrating object is still in place. Vascular control sometimes entails gaining exposure that is relatively distant from the site of injury due to a large surrounding hematoma. Vessel occlusion can then be achieved by various methods or devices, such as vascular tapes or loops, vascular clamps, direct pressure with a sponge stick or finger, or balloon occlusive devices. Although anticoagulation is routinely used in elective vascular procedures before obtaining vascular control, its use in the trauma setting is limited. It is typically contraindicated, as trauma patients usually present with multiorgan injuries with increased intracerebral or solid organ bleeding risks. In the situation where there is an isolated vascular injury, then anticoagulation can have a role. But this decision should be patient- or injury-specific, as combined vascular injuries are common and total control of venous bleeding might be difficult. Debridement of the injured segment of vessel is the initial step in vascular repair. Leaving damaged intima increases significantly the chance of post-repair thrombosis with all the attendant consequences. Remembering the pathophysiology described here about kinetic energy and cavitation effect, resection and debridement of the vessel might need to be extended beyond the site of obvious injury to include the total zone of damaged artery. External examination of the artery alone might not permit proper assessment of the extent of injury. For simple laceration of large vessels, lateral suture arteriorrhaphy can suffice if the vessel is large enough and the laceration is ⬍50% of the circumference. Smaller vessels or larger lacerations may require a patch angioplasty to prevent stenoses. Autogenous vein is the preferred patch material. A segmental resection with an end-to-end anastomosis can be performed for more complex injuries spanning a distance of ⬍1 cm. The ends should be spatulated to avoid anastomotic stricture, especially with small vessels. The key point, as in any vascular repair, is to produce a tension-free anastomosis. Usually, 3 cm of artery need to be mobilized for every 1 cm resected. For injuries ⬎1 cm, an interposition graft is usually required. The ideal conduit is the contralateral saphenous vein, if available. The ipsilateral saphenous vein should not be sacrificed if there is a concomitant ipsilateral venous injury because it is an important collateral venous return pathway. When autogenous vein is unavailable, prosthetic is an alternative and polytetraflouroethylene is most commonly used. However, wound contamination and soft-tissue injury limit the use of prosthetic grafts and patency rates are lower. Construction of spiral vein grafts is largely of historical interest.
Management of civilian and military vascular trauma The time required to make these grafts and the high thrombosis rates do not warrant their use.
Specific Injury Management Extremity Injuries The initial triage of extremity vascular injury follows the guidelines outlined here. Patients with hard signs of vascular injury are explored without any additional diagnostic imaging. If there is any concern regarding location, severity of injury, or thrombosis of the runoff vessels, then an intraoperative angiogram can be performed. When patients present with soft signs, variable strategies have been offered for management. In awake, mentally competent patients, serial physical examinations may suffice. Duplex scanning is a low-cost option to interrogate axial extremity vessels. Computed tomographic angiography has grown in popularity because of the availability of rapid thin-slice scanners, accuracy, and ability to evaluate for multisystem trauma.6 Surgical repair of an extremity vascular injury follows the principles and techniques described here. Anticoagulation should be given if it is reasonably safe, but significant softtissue injury or solid-organ injury usually preclude its use. Regional infusion of heparinized saline frequently suffices in lieu of systemic anticoagulation. Before completion of the repair, a Fogarty balloon catheter should be advanced proximally and distally to remove any thrombus. If any concerns exist about the integrity of the runoff vessels, intraoperative arteriography should be performed. Intraluminal shunting can be performed when vascular repair needs to be delayed due to unstable fracture requiring immediate fixation, resuscitation requirements, or the need to perform other life-saving procedures.6,7 This can be accomplished with various manufactured shunts, but any adequately sized sterile tubing can be used. Recent reports from the Iraq military conflict showed acceptable patency rates of up to 18 hours without anticoagulation. However, patency was dependent on location, with decreasing rates from 86% at proximal arteries to 12% at more distal locations.8 Shunt patency also depends on a number of technical factors. Chambers et al identified certain factors that contribute to shunt failure: insufficient venous outflow, untreated compartment syndrome, redundancy causing angulation or looping of the shunts, and inadequate length causing dislodgement.9
237 In upper-extremity brachial artery injury, severe ischemia is uncommon, as there are numerous collaterals. Isolated injury to either the radial or ulnar artery can be treated with ligation, as there should be adequate collateral perfusion from the other vessel unless the patient has an incomplete palmar arch. In cases where both forearm vessels are injured, then the ulnar should be revascularized because it is commonly the dominant vessel. Concomitant vascular and orthopedic injuries commonly pose a dilemma as to which repair takes precedence. Typically, vascular repair should be done before orthopedic repair in order to minimize ischemia time if there is not marked instability or shortening of the limb.10 The vascular repair must be evaluated for disruption before the final wound closure or undraping after the bony fixation is completed. When the integrity of a vascular repair may be compromised by a complex fracture fixation, then it may be ideal to temporarily revascularize with an intraluminal shunt.11,12 The definitive vascular repair is then performed after the orthopedic procedure. An alternative is expeditious placement of an external fixator before the definitive vascular repair. Despite all of these theoretical concerns, studies have shown that the surgical sequence does not affect the rate of amputations.13
Neck Injuries Neck injury poses a significant diagnostic and therapeutic dilemma. There are numerous vital structures in the very limited space extending from thoracic outlet to skull base. In addition to vascular structures, the aerodigestive tract and nerves are all at risk. The neck is divided into three anatomical zones to simplify the approach to cervical vascular trauma management (Table 2). Zone I extends from the thoracic outlet to the cricoid cartilage; Zone II from cricoid cartilage to the angle of the mandible; and Zone III from angle of the mandible to the base of the skull. Initial management and triage of cervical trauma is dependent of the zone and type of injury. As usual, hemodynamically unstable patients are immediately explored in the operating theater without diagnostic imaging other than cervical plain films. Exposure will depend on the zone of injury. Vascular control for Zone I and III are notoriously difficult due to anatomical constraints. For that reason, in hemodynamically stable patients, diagnostic imaging is recommended for the purpose of surgical planning. In
Table 2 Major Vessels of the Cervical Zones Zone I: Thoracic Outlet to Cricoid Common carotid artery Innominate artery (on the right) Subclavian artery and vein Internal jugular vein Aortic arch Innominate vein
Zone II: Cricoid to Angle of Mandible
Zone III: Angle of Mandible to Skull Base
Common, external, and internal carotid artery
Internal and external carotid artery
Vertebral artery Internal jugular vein
Vertebral artery Internal jugular vein
T. Nguyen, J. Kalish, and J. Woodson
238 addition, endovascular treatment of Zone I and III injuries may provide viable options that are less morbid. For Zone I, proximal control is obtained via a median sternotomy incision with extension of the incision on to the neck as necessary. The innominate and left common carotid artery can be controlled through this incision. The left proximal subclavian artery, on the other hand, usually requires a second or third left intercostal space anterolateral thoracotomy. A cervical incision along the anterior border of the sternocleidomastoid muscle is required for Zone II injury. If the bleeding is then found to be from a more proximal source, then the cervical incision can be extended into a median sternotomy. In the situation of bilateral cervical vascular injuries, either a transverse Kocher incision or bilateral cervical incisions will gain exposure to both carotids. When exposure of Zone III is required, subluxation or resection of the angle of the mandible and resection of the posterior belly of the digastric muscle may be necessary (Table 3). Even so, control of the distal internal carotid artery may still be difficult. Other methods to gain distal control are balloon occlusive devices through the common carotid artery or site of injury. Due to the difficulty in exposure and control of Zone III injuries, endovascular treatment is the preferred option when feasible. Surgical options for the management of carotid injuries include ligation or repair (primary, patch angioplasty, or bypass). The external carotid artery and internal jugular vein usually can be ligated with impunity. Ligation of the internal carotid artery can be associated with significant morbidity and is usually performed when no other surgical options are available.14,15 If primary internal carotid artery repair is not possible, there are several reconstruction options. The external carotid artery can be used as a conduit by dividing it and transposing the proximal end to the internal carotid artery. Otherwise, an interposition graft can be constructed with saphenous vein or rarely with prosthetic graft. Shunting should be use if there are concerns regarding collateral perfusion from the Circle of Willis. Treatment for blunt cervical vascular trauma usually involves a nonoperative approach. Blunt cervical vascular injuries are less frequent, with an incidence of 0.6% in an unscreened versus up to 25% in a screened blunt trauma population.16 Computed tomographic angiography has been accepted as the screening modality for blunt cervical vascular
injury, as it compares favorably with conventional angiography.17 The majority of blunt cervical vascular injuries only requires medical treatment with either antiplatelet or anticoagulation therapy for 3 to 6 months, but the optimal agent is unknown because there are no randomized controlled study comparing the two.18 Recent meta-analyses showed no difference between antiplatelet agents and warfarin.19,20 Indications for invasive therapy include progression of neurologic symptoms, persistence of pseudoaneurysm despite antithrombotic treatment, and worsening chronic dissection. The choice of therapy, endovascular or open, is dependent on location of injury, contraindication to antithrombotic therapy, and compliance with follow-up. Surgical repair can usually be done primarily or with patch angioplasty. Vertebral artery injury is a rare occurrence, with an incidence of up to 0.77% of all trauma admissions. Medical treatment for blunt injuries with antithrombotic agents is identical to treatment for carotid artery injury. In fact, most case series describe both carotid and vertebral artery injuries simultaneously.20 Exposure of the vertebral artery depends on the particular segment injured. The most accessible segment is the first segment (V1), which begins at the origin and ends at C6. Exposure requires dividing the sternocleidomastoid and anterior scalene muscle from their thoracic outlet attachments. The phrenic nerve is at risk in this area. The second segment (V2) travels through C6 to C2 transverse foramens and requires resection of the anterior transverse process. This dissection is hazardous because of the adjacent nerve roots and an extensive venous network. In addition, the artery in this segment is deficient in the external elastic lamina and fragile. The third segment (V3) begins at C2 and travels to the skull base. Exposure requires extending the cervical incision posteriorly to the mastoid process. The sternocleidomastoid muscle is divided with care not to injure the spinal accessory nerve. The lateral process of C1 also needs to be resected to gain access to the V3. The fourth segment (V4) is intracranial, as it travels along the brainstem to join the contralateral vertebral artery. Because of these difficult and hazardous exposures, surgical treatment of vertebral artery hemorrhage is best treated with ligation at V1. Continued bleeding from the other segments can be temporarily treated with bone wax packings or balloon occlusive devices before definitive endoluminal embolization at the distal end of the vessel.21
Table 3 Exposure Incisions for Cervical and Great Vessels Injury Zone III Posteriorly to mastoid process with subluxation of mandible Cervical (anterior border of SCM) Supraclavicular Infraclavicular Median sternotomy 2nd or 3rd ICS left anterolateral thoracotomy
Zone I
Proximal Subclavian
ⴙ
ⴙ/ⴚ ⴙ/ⴚ
ⴙ/ⴚ ⴙ/ⴚ (left subclavian)
ⴙ/ⴚ
ⴙ
ⴙ (right subclavian) ⴙ (left subclavian)
Zone II
Distal Subclavian
Axillary
ⴙ ⴙ/ⴚ
ⴙ/ⴚ ⴙ
ⴙ ⴙ
Abbreviations: ICS, intercostal space; SCM, sternocleidomastoid muscle.
Management of civilian and military vascular trauma
Axillosubclavian Injuries Injury to the subclavian vessels has a high morbidity and mortality. Demetriades et al documented a 61% prehospital and 15.5% perioperative mortality rate in their series of 228 penetrating subclavian vessel injuries.22 Surgical dissection in the thoracic outlet region is highly morbid due to the adjacent brachial plexus, surrounding hematoma, and associated pulmonary and mediastinal injuries of these traumatic injuries. Therefore, it is usually necessary for hemodynamically unstable patients only. In stable patients, it is prudent to obtain imaging before therapy, usually with computed tomographic angiography. This allows evaluation of associated cervical, thoracic, and mediastinal injuries. But the “gold standard” is conventional angiography because of its potential for diagnosis and therapy. Because of the morbidity concerns of surgical treatment, endovascular treatment has evolved into the ideal therapy in the hemodynamically stable patient. Even if surgical repair is indicated, a large compliant occlusion balloon can be placed at the time of angiography for proximal control. If indicated in an unstable patient, the subclavian artery can be ligated without resulting in severe ischemia due to the abundance of collaterals. If limiting claudication occurs the artery can be reconstructed electively.23-25 Exposure of the right subclavian artery or innominate artery for proximal control is through a median sternotomy. The proximal left subclavian artery is accessed with a high anterolateral thoracotomy in the second or third intercostal space. The clavicle can be resected as needed. Distal subclavian exposure requires a supraclavicular incision. Isolated axillary artery injury can be treated with an infraclavicular incision, but proximal control usually requires exposure of the subclavian artery (Table 3).
Aortic and Caval Injuries Aortic injury (predominantly located at the isthmus) is the second most common cause of death in blunt trauma.26 Parmley et al advocated urgent surgery in this patient population as they had a 61% 7-day mortality rate in their series.27 The treatment paradigm has shifted since then to a nonoperative approach in hemodynamically stable patients, with several studies showing no increase in survival with early surgery.28-30 Blood pressure control should be the initial treatment goal. Simon and Leslie identified several risk factors for failure of conservative management: increasing mediastinal hematoma or pleural effusion, extravasation of contrast, malperfusion complications, and hypotension.31 Surgical repair of the descending thoracic aorta requires a left thoracotomy. After obtaining proximal and distal control, repair of injury is standard with primary or, more often, interposition graft repair. Distal aortic perfusion during aortic clamping is usually required and can be via a left atrial to distal aorta, right atrium to femoral artery, or femoral artery to femoral vein bypass. Repair of the great vessels can be performed with interposition grafts via side-biting vascular clamps without the need for cardiopulmonary bypass. Exposures were described in earlier sections.
239 The vascular abdomen is divided into three retroperitoneal zones. Zone I is the midline and includes the supramesocolic vasculature (celiac trunk, superior mesenteric artery, renal arteries, inferior vena cava (IVC) and its branches, suprarenal aorta) and the inframesocolic vasculatures (inferior mesenteric artery, IVC, infrarenal aorta). Zone II is the perinephric regions. Zone III is the pelvic region and includes the iliac vessels. Management of abdominal vascular trauma depends on the type and location of injury. Exposure of the supramesocolic Zone I entails mobilization and medial rotation the left colon, spleen, tail of pancreas, stomach, and possibly left kidney. This will gain exposure to the aorta, celiac, superior mesenteric artery, and left renal artery. Mobilization and medial rotation of the right colon, duodenum, and head of pancreas will expose the right renal artery and supramesocolic IVC. The inframesocolic Zone I is exposed by retracting the mesocolon cephalad and small bowel to the right and dividing the parietal peritoneum overlying the aorta or IVC. Mobilization and medial rotation of the right colon, duodenum, and head of pancreas or left colon will also gain access to the right and left Zone II, respectively. Medial rotation of the right or left colon will also allow exposure of Zone III inferiorly. Surgical treatment of the specific vessel injury follows the basic principles of vascular surgery. Primary repair can be done with lateral arteriorraphy or end-to-end anastomosis, if possible. If reconstruction is required, then autogenous vein or polytetraflouroethylene are both optional conduits. In the setting of enteric contamination, it is not desirable but permissible in life-saving situations to use polytetraflouroethylene, but copious irrigation and vascularized tissue coverage of the anastomosis is imperative.32 Ligation of the celiac trunk (or its branches) or the inferior mesenteric artery is usually benign. On the other hand, ligation of the superior mesenteric artery has significant risk of extensive bowel ischemia. Zone II hematoma in blunt trauma should not be explored unless it is expanding. On the contrary, all penetrating trauma Zone II hematomas should be explored. Treatment options include nonoperative, revascularization, or nephrectomy. Revascularization of occluded renal arteries should not be attempted unless ischemia time is less than 6 hours, there are bilateral renal injuries, or there is injury to a solitary kidney.33-35 Zone III hematomas should be explored if due to a penetrating injury, or to a blunt injury with a resulting expanding hematoma or an abnormal femoral pulse. Ligation of common or external iliac is not tolerable and should not be done. In damage-control situations, intraluminal shunting is advisable. As with extremity vascular injuries, development of compartment syndrome is possible and patients should be monitored; and there should be a low threshold for fasciotomy. Vena caval injury can usually be repaired primarily with lateral venorrhaphy, but patch angioplasty and polytetraflouroethylene interposition graft may be necessary for larger injuries. The key is to avoid a subsequent stenosis after the repair, which is at risk of developing thrombosis or embolism; a temporary IVC filter may be required in such a case.
240 Ligation of the infrarenal IVC may be tolerated and necessary in unstable patients, but all suprarenal IVC injuries must be repaired due to the frequent occurrence of hemodynamic instability secondary to drop in preload and significant risk of renal failure with ligation at this level.36 Exposure of the retrohepatic vena cava is very difficult. A retrohepatic hematoma is the only exception to mandatory exploration of all penetrating trauma hematoma. Perihepatic packing is the first-line treatment, and can be left in place for 24 to 48 hours before a second-look operation. If all else fails, then atriocaval shunting, total hepatic vascular isolation, or division of the liver to gain exposure can be attempted for hemorrhage control.
Iatrogenic Injury Iatrogenic vascular injury is an increasing problem, comprising up to 33% of the current civilian vascular trauma patient population.37,38 The rise of iatrogenic vascular injury results from more frequent catheter-based therapies. Of these, 60% are due to femoral access complications and 27% are intraoperative injuries.4 Aside from percutaneous access complications, these injuries are also associated with orthopedic and spine procedures.39 Wood et al40 systematically reviewed 40 articles that reported the frequency of vascular injury with anterior lumbosacral spine surgery. The overall vascular complication rate was 5% (range, 0 to 18%), and venous injury was more common than arterial injury (up to 18% v 5%). The most common vessels injured were the left common iliac vein, IVC, and iliolumbar vein, usually due to retraction of the vessels. Procedural risk factors were L4-L5 exposure, revision surgery, transperitoneal approach, and laparoscopic technique. The authors recommended having a vascular surgeon available when these risk factors were present.40 More of these iatrogenic injuries are requiring invasive therapy to either treat or prevent complications. Guilbert et al41 reported a case series of 13 patients who had either carotid or subclavian artery cannulation with ⱖ7Fr catheter during internal jugular vein central line placements. Five patients were treated with a “pull and pressure” method of manual compression. All had subsequent complications of bleeding, stroke, or death. Eight patients, on the other hand, were treated with either open repair or an endovascular approach of catheter removal, and none had complications. They performed a meta-analysis comprising 30 patients with internal jugular vein line misplacement. Seventeen patients were treated with the pull/pressure method, and 13 patients were treated with open or endovascular repair. All eight patients who developed complications (airway compromise due to hematoma, pseudoaneurysm, hemothorax, and death) were from the pull/pressure group.41
War and Vascular Trauma The first recorded attempts at repair of arterial injuries were during World War I by Croatian surgeons, but the techniques used remain unknown. Long evacuation times for casualties, sepsis, and poor instruments also limited interest
T. Nguyen, J. Kalish, and J. Woodson and feasibility of repairing injured vessels. Debakey and Simeone reviewed the results of 2,471 vascular injuries resulting from World War II and documented a 50% amputation rate when ligation of injured vessels was performed.42 Despite this appalling high rate of amputation, they still concluded that arterial repair was not warranted in most cases because of the high complication rates secondary to sepsis and thrombosis. The Korean conflict was marked by the US Army Fielding Mobile Army Surgical Hospitals (MASH units) and surgical research teams. Casualty evacuation times were improved with the use of helicopters, and antibiotics were more plentiful than in previous wars. These conditions permitted special surgical teams to explore the potential repair of vascular injuries and document a decline in extremity amputation rate from the 50% seen in World War II to 13% when vascular injuries were repaired. The Vietnam War marked advances in the utilization of helicopters for transporting troops and wounded soldiers. Combat medics were better trained to control hemorrhage and specialized centers were identified by the US Army to treat and evaluate vascular injuries. Colonel Norman Rich established the Vietnam Vascular Registry at Walter Reed Army Hospital. This registry helped define the optimal algorithms for managing patients with vascular trauma, such as the importance of repairing a venous injury occurring concomitantly with a popliteal artery injury to improve patency rates of the arterial repair. As previously stated, the advancement in management of vascular trauma has been written in the history of the wars of the past century. At the time of the writing of this article, America has been at war for a decade and old lessons about the management of vascular trauma have been reinforced and new lessons have been learned. The wars in Afghanistan (Operation Enduring Freedom) and Iraq (Operation Iraqi Freedom) have been marked by advances in technology, tactical and strategic evacuation (flying intensive care units), and application of body armor. The US Army has developed and fielded a new advanced combat action tourniquet, resuscitation protocols, smaller (20-person) and more mobile trauma resuscitation teams (Forward Surgical Teams), and a Joint Theater Trauma Registry that allows rapid improvement in care. In addition, there has been improvement in the training of medics, surgeons, and trauma teams. All of these improvements have contributed to the lowest case fatality rates in the history of modern warfare. A soldier injured in battle has a ⬎97% chance of surviving if they make it to a Forward Surgical Team. A standard has been set in the combat zone that all injured soldiers will receive Trauma Center Level care within the first “golden hour” defined by civilian trauma systems. The signature injury-producing weapon of Operation Iraqi Freedom and Operation Enduring Freedom is the improvised explosive device. Improvement in protective body and vehicle armor has contributed to soldier survivability, but the rate of extremity trauma is now higher in survivors than previously reported in earlier wars. Extremity injury now accounts for 40% to 70% of all combat wounds, with 70% of
Management of civilian and military vascular trauma extremity injuries occurring on the lower extremities. Vascular injuries occur in 5% to 7% of all those injured on the battlefield. Clouse et al reviewed the current status of vascular trauma in wartime using the Balad Vascular Registry from Iraq.43 They noted that cervical vascular injuries accounted for 16% of vascular trauma, with carotid injuries constituting nearly three-quarters (73%) of this group. They also reported an increased use of temporary vascular shunts to perfuse limbs, while other priorities were addressed or while patients were transported to a higher level of care. Eighty-six percent of shunts remained patent during their period of use without anticoagulants. Extensive soft-tissue and bony injuries (reflected in a high Mangled Extremity Severity Score) were the primary reasons for limb loss, rather than inability to revascularize the limb. The management strategy of rapid evacuation, temporary shunting, and early definitive vascular repair in the combat zone has resulted in excellent limb-salvage rates. The recent wars have produced only a limited experience with endovascular management of vascular trauma. Isolated subclavian artery and carotid-jugular fistula repairs with stent grafts have been reported. The long logistical trail, varying endovascular abilities of surgeons, and multiple injuries of victims have limited the application of endovascular techniques. These issues are now being analyzed. The ability to rapidly evacuate critically ill soldiers from the combat zone using Critical Care Air Transport Teams within hours to days after wounding increases the possibility of applying endovascular therapies at medical centers remote from the battlefield. There have been ⬎30,000 casualties, with only 1,200 amputations resulting from Operation Iraqi Freedom and Operation Enduring Freedom. Limb salvage revascularization surgery, coupled with superb rehabilitation programs, has returned hundreds of soldiers and civilians injured on the battlefield to productive lives. If war is the dark side of humanity, then the advances in medical care resulting from this experience represent the hope for humanity.
Conclusions The tenets of management of vascular trauma have evolved from the many lessons that can be traced through different time periods, different wars, and different battlefields across the world. Vascular surgical care will always rely on the basic premise of “stopping the bleeding,” and restoring perfusion. Although open surgical management has always been the gold standard for dealing with vascular trauma, the use of endovascular techniques is becoming more prominent for selected indications. The benefits and detriments of these newer technologies will require constant reevaluation to arrive at the optimal care algorithms as the future unfolds.
References 1. Rich NM, Hughes CW: Vietnam vascular registry: a preliminary report. Surgery 65:218-226, 1969 2. Rich NM, Baugh JH, Hughes CW: Acute arterial injuries in Vietnam: 1,000 cases. J Trauma 10:359-369, 1970 3. Centers for Disease Control and Prevention, National Center for Health Statistics: National Vital Statistics System. Available at: http://www.
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cdc.gov/injury/wisqars/LeadingCauses.html. Accessed December 8, 2010 Giswold ME, Landry GJ, Taylor LM, Moneth GL: Iatrogenic arterial injury is an increasingly important cause of arterial trauma. Am J Surg 187:590-592, 2004 Bongard F, Dubrow T, Klein S: Vascular injuries in the urban battleground: experience at a metropolitan trauma center. Ann Vasc Surg 4:415-418, 1990 Feliciano DV: Management of peripheral arterial injury. Curr Opin Crit Care Sept 16, 2010 [Epub ahead of print] Rozycki GS, Tremlay LN, Feliciano DV, McClelland WB: Blunt vascular trauma in the extremity: diagnosis, management, and outcome. J Trauma 55:814-824, 2003 Rasmussen TE, Clouse WD, Jenkins DH, Peck MA, Eliason JL, Smith DL: The use of temporary vascular shunts as a damage control adjunct in the management of wartime vascular injury. J Trauma 61:8-12, 2006 Chambers LW, Green DJ, Sample K, et al: Tactical surgical intervention with temporary shunting of peripheral vascular trauma sustained during Operation Iraqi Freedom: one unit’s experience. J Trauma 61:824830, 2006 Romanoff H, Goldberger S: Combined severe vascular and skeletal trauma: management and results. J Cardiovasc Surg 20:493-498, 1979 Glass GE, Pearse MF, Nanchahal J: Improving lower limb salvage following fractures with vascular injury: a systematic review and new management algorithm. J Plast Reconstr Aesthet Surg 62:571-579, 2009 McHenry TP, Holcomb JB, Aoki N, Lindsey RW: Fractures with major vascular injuries from gunshot wounds: implications of surgical sequence. J Trauma 53:717-721, 2002 Fowler J, MacIntyre N, Rehman S, Gaughan JP, Leslie S: The importance of surgical sequence in the treatment of lower extremity injuries with concomitant vascular injury: a meta-analysis. Injury 40:72-76, 2009 du Toit DF, van Schalkwyk GD, Wadee SA, Warren BL: Neurologic outcome after penetrating extracranial arterial trauma. J Vasc Surg 38: 257-262, 2003 Rao PM, Ivatury RR, Sharma P, Vinzons AT, Nassoura Z, Stahl WM: Cervical vascular injuries: a trauma center experience. Surgery 114: 527-531, 1993 Biffl WL, Moore EE, Ryu RK, et al: The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg 228:462-470, 1998 Eastman AL, Chason DP, Perez CL, McAnulty AL, Minei JP: Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime? J Trauma 60:925-929, 2006 Bromberg WJ, Collier BC, Diebel LN, et al: Blunt cerebrovascular injury practice management guidelines: the Eastern Association for the Surgery of Trauma. J Trauma 68:471-477, 2010 Lyrer P, Engelter S: Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev 6:10:CD000255, 2010 Menon R, Kerry S, Norris JW, Markus HS: Treatment of cervical artery dissection: a systematic review and meta-analysis. J Neurol Neurosurg Psychiatry 79:1122-1127, 2008 Miller PR, Fabian TC, Bee TK, et al: Blunt cerebrovascular injuries: diagnosis and treatment. J Trauma 51:279-285, 2001 Demetriades D, Rabinowitz B, Pezikis A, Franklin J, Palexas G: Subclavian vascular injuries. Br J Surg 74:1001-1003, 1987 Rich NM, Hobson RW, Jarstfer BS, Geer TM: Subclavian artery trauma. J Trauma 13:485-496, 1973 Levin PM, Rich NM, Hutton JE: Collateral circulation in arterial injuries. Arch Surg 102:392-399, 1971 Graham JM, Mattox KL, Feliciano DV, Debakey ME: Vascular injuries of the axilla. Ann Surg 195:232-238, 1982 Fabian TC, Richardson JD, Croce MA, et al: Prospective study of blunt aortic injury: multicenter trial of the American Association for the Surgery of Trauma. J Trauma 42:374-380, 1987 Parmley LF, Mattingly TW, Manion WC, Jahnke EJ: Nonpenetrating traumatic injury of the aorta. Circulation 17:1086-1101, 1958 Holmes JH, Bloch RD, Hall RA, Carter YM, Karmy-Jones RC: Natural
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29.
30.
31. 32. 33. 34. 35.
history of traumatic rupture of the thoracic aorta managed nonoperatively: a longitudinal analysis. Ann Thorac Surg 2002;73:11491154, 2002 Camp PC, Shackford SR: Outcome after blunt traumatic aortic laceration: identification of a high-risk cohort. The Western Trauma Association Multicenter Group. J Trauma 43:413-422, 1997 Maggisano R, Nathens A, Alexandrova NA, et al: Traumatic rupture of the thoracic aorta: should one always operate immediately? Ann Vasc Surg 9:44-52, 1995 Simon BJ, Leslie C: Factors predicting early in-hospital death in blunt thoracic aortic injury. J Trauma 51:906-910, 2001 Accola KD, Feliciano DV, Mattox KL, et al: Management of injuries to the suprarenal aorta. Am J Surg 154:613-618, 1987 Haas CA, Spirnak JP: Traumatic renal artery occlusion: a review of the literature. Tech Urol 4:1-11, 1998 Tillou A, Romero J, Asensio JA, et al: Renal vascular injuries. Surg Clin North Am 81:1417-1430, 2001 Lock JS, Carraway RP, Hudson HC, Laws HL: Proper management of renal artery injury from blunt trauma. South Med J 78:406-410, 1985
36. Sullivan PS, Dente CJ, Patel S, et al: Outcome of ligation of the inferior vena cava in the modern era. Am J Surg 199:500-506, 2010 37. Rich NM, Hobson RW, Fedde CW: Vascular trauma secondary to diagnostic and therapeutic procedures. Am J Surg 128:715-721, 1974 38. Youkey JR, Clagett GP, Rich NM, et al: Vascular trauma secondary to diagnostic and therapeutic procedure: 1974 through 1982. A comparative review. Am J Surg 146:788-791, 1983 39. Lazarides MK, Arvanitis DP, Dayantas JN: Iatrogenic arterial trauma associated with hip joint surgery: an overview. Eur J Vasc Surg 5:549556, 1991 40. Wood KB, Devine J, Fischer D, Dettori JR, Janssen M: Vascular injury in elective anterior lumbosacral surgery. Spine 35:S66-S75, 2010(suppl) 41. Guilbert MC, Elkouris S, Bracco D, et al: Arterial trauma during central venous catheter insertion: case series, review and proposed algorithm. J Vasc Surg 48:918-925, 2008 42. Debakey ME, Simeone FA: Battle injuries of the arteries in World War II: an analysis of 2,471 cases. Ann Surg 123:534-579, 1946 43. Clouse WD, Rasmussen TE, Peck MA, et al: In-theater management of vascular injury: 2 years of the Balad Vascular Registry. J Am Coll Surg 204:625-632, 2007
H
IPPOCRATES IS CREDITED with saying, “he who wishes to be a surgeon should go to war,” and its truth is evident in the origins and development of current vascular surgical trauma care. Wars have always produced large numbers of sick and wounded, which challenged physicians to improve the practice of medicine and surgery through development of new procedures, therapies, systems, and paradigms for care. Boiling oil and cautery of ancient wars gave way to arterial ligation. Better sanitation and shorter, improved evacuation systems allowed the appropriate conditions to develop techniques to repair arteries. Ligation of injured vessels was still the predominant method of handling vascular trauma through the end of World War II. Arterial repairs and vein bypass grafting, resulting in a decrease in amputation rates (50% to 13%) and greater advances in limb salvage, arrived with the advent of mobile surgical hospitals and vascular specialty centers from the Korean and Vietnam Wars. Through the Vietnam Vascular Registry, a large volume of data was collected and analyzed, which led to development of best practices in the management of vascular trauma. The military lessons were disseminated to and further refined in the civilian sector.1,2 Modern-day civilian trauma algorithms are rooted in the lessons learned on the many battlefields across the world.
Epidemiology Trauma remains the leading cause of death in the 15- to 44-year-old age group in the United States, as a consequence
Boston Medical Center, Boston, MA. Address reprint requests to: Jeffrey A Kalish, Boston Medical Center, 88 East Newton Street, Collamore 5, D-506, Boston, MA 02118. E-mail: [email protected]: [email protected]
0895-7967/$-see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1053/j.semvascsurg.2010.11.004
of unintentional injury, assault, homicide, and suicide.3 The distribution of civilian vascular trauma has not changed much throughout the decades; penetrating trauma is still the predominant etiology (70% to 80%), while blunt trauma constitutes 5% to 15% of injuries. Of the penetrating injuries, most (50% to 80%) are sustained from gunshot wounds, and stab wounds are less prevalent (10% to 30%). In addition, iatrogenic vascular injury has been increasing in prevalence as the number of invasive procedures increases. In fact, it has been described as high as 33% of all vascular trauma at a Level I trauma center.4 Overall, arteries are more often injured than veins, and extremities are injured more than other anatomical regions (similar to reported military experiences).5
Pathophysiology Successful management and treatment of vascular injuries requires an understanding of the pathophysiology and biomechanics of vascular trauma. On a simplistic level, vascular trauma is categorized into two types: blunt or penetrating. However, the severity of injury is a consequence of multiple factors: (1) direct injury to vessels from missiles or penetrating objects; (2) the transfer of energy and heat to tissues (kinetic energy). This results in cavitation effect (shock wave) of high-velocity moving objects as it penetrates tissues and will cause a zone of injury at a distance from the path of the missile tract; (3) the shearing or compressive forces of rapid deceleration in the case of blunt trauma. This can lead to contusion, tearing, thrombosis, intimal flap, and dissection of blood vessels; and (4), although uncommon, the embolization of foreign objects (fragments, shotgun pellets, or bullets), which can potentially cause distal vessel injury, occlusion, or thrombosis. 235
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Basic Principles of Open Management of Vascular Trauma Management of vascular trauma begins with the initial triage, evaluation, and resuscitation of the trauma patient. Appropriate attention must be paid to the airway, ventilation, and external hemorrhage control, and circulating blood volume should be restored. Immediate hemorrhage control can often be obtained by direct pressure or application of tourniquets on extremities. Once hemorrhage is controlled, then resuscitation is continued through the remaining primary and secondary survey in accordance with Advanced Trauma Life Support protocols to identify and prioritize all associated injuries. The patient with multiple injuries needs detailed assessment before embarking on complex or lengthy vascular repairs. Unrecognized severe intraabdominal or intracranial injuries can lead to disastrous outcomes if not addressed early. Pericardial effusions and cardiac contusions can render the patient too unstable to proceed with complex repairs. Vascular shunts have been used with increasing frequency to permit temporary reperfusion of extremities while other injuries are treated. Diagnosing vascular injury without any obvious source of external hemorrhage is more challenging. Signs and symptoms of arterial injury can be described as “hard” and “soft” (Table 1). Hard signs, such as active arterial hemorrhage, expanding hematoma, loss of distal pulse, signs of ischemia, and a bruit or thrill are highly suggestive of arterial injury. Profound signs of ischemia include the classic 6 “Ps”: paresthesia, paralysis, pulselessness, pain, pallor, and poikilothermia. With such findings, no diagnostic imaging is usually required before surgical exploration of extremity vessels. Soft signs raise the suspicion of arterial injury and include moderate-sized hematoma, history of significant blood loss or hypotension at the prehospital scene, proximity of wound to vascular structures or bony injuries, diminished distal pulses, and ipsilateral neurologic deficits. Soft signs can warrant additional diagnostic imaging, duplex studies or observation with repeated interval physical examination. Ankle-brachial index (ABI) is an objective bedside diagnostic procedure that is instrumental in the management of lower-extremity trauma patient. An ABI of ⬍0.9 may suggest arterial injury and need for further diagnostic imaging.6 A
Table 1 Clinical Signs of Arterial Injury: Hard Signs Warrant Surgical Exploration and Control, Soft Signs Afford Time for Further Diagnostic Imaging Hard
Soft
Arterial bleeding Loss of pulse Expanding hematoma Bruit or thrill
History of prehospital blood loss Diminished pulse Moderate hematoma Proximity to large vessel or bony injury Signs of ischemia (6 Ps*) Ipsilateral neurologic deficit *Paresthesia, paralysis, pulselessness, pain, pallor, and poikilothermia.
good history and examination of the uninjured contralateral limb is important for interpreting ABIs. Older patients with peripheral vascular disease may present with reduced ABIs, confusing the issue. Once the decision for operative repair has been made, the basic principles for management of vascular trauma apply irrespective of types and location of injury. Before exploring the injured vessel, proximal and distal control must be obtained. This is especially important in injuries that have ceased bleeding due to an adherent clot or if the offending penetrating object is still in place. Vascular control sometimes entails gaining exposure that is relatively distant from the site of injury due to a large surrounding hematoma. Vessel occlusion can then be achieved by various methods or devices, such as vascular tapes or loops, vascular clamps, direct pressure with a sponge stick or finger, or balloon occlusive devices. Although anticoagulation is routinely used in elective vascular procedures before obtaining vascular control, its use in the trauma setting is limited. It is typically contraindicated, as trauma patients usually present with multiorgan injuries with increased intracerebral or solid organ bleeding risks. In the situation where there is an isolated vascular injury, then anticoagulation can have a role. But this decision should be patient- or injury-specific, as combined vascular injuries are common and total control of venous bleeding might be difficult. Debridement of the injured segment of vessel is the initial step in vascular repair. Leaving damaged intima increases significantly the chance of post-repair thrombosis with all the attendant consequences. Remembering the pathophysiology described here about kinetic energy and cavitation effect, resection and debridement of the vessel might need to be extended beyond the site of obvious injury to include the total zone of damaged artery. External examination of the artery alone might not permit proper assessment of the extent of injury. For simple laceration of large vessels, lateral suture arteriorrhaphy can suffice if the vessel is large enough and the laceration is ⬍50% of the circumference. Smaller vessels or larger lacerations may require a patch angioplasty to prevent stenoses. Autogenous vein is the preferred patch material. A segmental resection with an end-to-end anastomosis can be performed for more complex injuries spanning a distance of ⬍1 cm. The ends should be spatulated to avoid anastomotic stricture, especially with small vessels. The key point, as in any vascular repair, is to produce a tension-free anastomosis. Usually, 3 cm of artery need to be mobilized for every 1 cm resected. For injuries ⬎1 cm, an interposition graft is usually required. The ideal conduit is the contralateral saphenous vein, if available. The ipsilateral saphenous vein should not be sacrificed if there is a concomitant ipsilateral venous injury because it is an important collateral venous return pathway. When autogenous vein is unavailable, prosthetic is an alternative and polytetraflouroethylene is most commonly used. However, wound contamination and soft-tissue injury limit the use of prosthetic grafts and patency rates are lower. Construction of spiral vein grafts is largely of historical interest.
Management of civilian and military vascular trauma The time required to make these grafts and the high thrombosis rates do not warrant their use.
Specific Injury Management Extremity Injuries The initial triage of extremity vascular injury follows the guidelines outlined here. Patients with hard signs of vascular injury are explored without any additional diagnostic imaging. If there is any concern regarding location, severity of injury, or thrombosis of the runoff vessels, then an intraoperative angiogram can be performed. When patients present with soft signs, variable strategies have been offered for management. In awake, mentally competent patients, serial physical examinations may suffice. Duplex scanning is a low-cost option to interrogate axial extremity vessels. Computed tomographic angiography has grown in popularity because of the availability of rapid thin-slice scanners, accuracy, and ability to evaluate for multisystem trauma.6 Surgical repair of an extremity vascular injury follows the principles and techniques described here. Anticoagulation should be given if it is reasonably safe, but significant softtissue injury or solid-organ injury usually preclude its use. Regional infusion of heparinized saline frequently suffices in lieu of systemic anticoagulation. Before completion of the repair, a Fogarty balloon catheter should be advanced proximally and distally to remove any thrombus. If any concerns exist about the integrity of the runoff vessels, intraoperative arteriography should be performed. Intraluminal shunting can be performed when vascular repair needs to be delayed due to unstable fracture requiring immediate fixation, resuscitation requirements, or the need to perform other life-saving procedures.6,7 This can be accomplished with various manufactured shunts, but any adequately sized sterile tubing can be used. Recent reports from the Iraq military conflict showed acceptable patency rates of up to 18 hours without anticoagulation. However, patency was dependent on location, with decreasing rates from 86% at proximal arteries to 12% at more distal locations.8 Shunt patency also depends on a number of technical factors. Chambers et al identified certain factors that contribute to shunt failure: insufficient venous outflow, untreated compartment syndrome, redundancy causing angulation or looping of the shunts, and inadequate length causing dislodgement.9
237 In upper-extremity brachial artery injury, severe ischemia is uncommon, as there are numerous collaterals. Isolated injury to either the radial or ulnar artery can be treated with ligation, as there should be adequate collateral perfusion from the other vessel unless the patient has an incomplete palmar arch. In cases where both forearm vessels are injured, then the ulnar should be revascularized because it is commonly the dominant vessel. Concomitant vascular and orthopedic injuries commonly pose a dilemma as to which repair takes precedence. Typically, vascular repair should be done before orthopedic repair in order to minimize ischemia time if there is not marked instability or shortening of the limb.10 The vascular repair must be evaluated for disruption before the final wound closure or undraping after the bony fixation is completed. When the integrity of a vascular repair may be compromised by a complex fracture fixation, then it may be ideal to temporarily revascularize with an intraluminal shunt.11,12 The definitive vascular repair is then performed after the orthopedic procedure. An alternative is expeditious placement of an external fixator before the definitive vascular repair. Despite all of these theoretical concerns, studies have shown that the surgical sequence does not affect the rate of amputations.13
Neck Injuries Neck injury poses a significant diagnostic and therapeutic dilemma. There are numerous vital structures in the very limited space extending from thoracic outlet to skull base. In addition to vascular structures, the aerodigestive tract and nerves are all at risk. The neck is divided into three anatomical zones to simplify the approach to cervical vascular trauma management (Table 2). Zone I extends from the thoracic outlet to the cricoid cartilage; Zone II from cricoid cartilage to the angle of the mandible; and Zone III from angle of the mandible to the base of the skull. Initial management and triage of cervical trauma is dependent of the zone and type of injury. As usual, hemodynamically unstable patients are immediately explored in the operating theater without diagnostic imaging other than cervical plain films. Exposure will depend on the zone of injury. Vascular control for Zone I and III are notoriously difficult due to anatomical constraints. For that reason, in hemodynamically stable patients, diagnostic imaging is recommended for the purpose of surgical planning. In
Table 2 Major Vessels of the Cervical Zones Zone I: Thoracic Outlet to Cricoid Common carotid artery Innominate artery (on the right) Subclavian artery and vein Internal jugular vein Aortic arch Innominate vein
Zone II: Cricoid to Angle of Mandible
Zone III: Angle of Mandible to Skull Base
Common, external, and internal carotid artery
Internal and external carotid artery
Vertebral artery Internal jugular vein
Vertebral artery Internal jugular vein
T. Nguyen, J. Kalish, and J. Woodson
238 addition, endovascular treatment of Zone I and III injuries may provide viable options that are less morbid. For Zone I, proximal control is obtained via a median sternotomy incision with extension of the incision on to the neck as necessary. The innominate and left common carotid artery can be controlled through this incision. The left proximal subclavian artery, on the other hand, usually requires a second or third left intercostal space anterolateral thoracotomy. A cervical incision along the anterior border of the sternocleidomastoid muscle is required for Zone II injury. If the bleeding is then found to be from a more proximal source, then the cervical incision can be extended into a median sternotomy. In the situation of bilateral cervical vascular injuries, either a transverse Kocher incision or bilateral cervical incisions will gain exposure to both carotids. When exposure of Zone III is required, subluxation or resection of the angle of the mandible and resection of the posterior belly of the digastric muscle may be necessary (Table 3). Even so, control of the distal internal carotid artery may still be difficult. Other methods to gain distal control are balloon occlusive devices through the common carotid artery or site of injury. Due to the difficulty in exposure and control of Zone III injuries, endovascular treatment is the preferred option when feasible. Surgical options for the management of carotid injuries include ligation or repair (primary, patch angioplasty, or bypass). The external carotid artery and internal jugular vein usually can be ligated with impunity. Ligation of the internal carotid artery can be associated with significant morbidity and is usually performed when no other surgical options are available.14,15 If primary internal carotid artery repair is not possible, there are several reconstruction options. The external carotid artery can be used as a conduit by dividing it and transposing the proximal end to the internal carotid artery. Otherwise, an interposition graft can be constructed with saphenous vein or rarely with prosthetic graft. Shunting should be use if there are concerns regarding collateral perfusion from the Circle of Willis. Treatment for blunt cervical vascular trauma usually involves a nonoperative approach. Blunt cervical vascular injuries are less frequent, with an incidence of 0.6% in an unscreened versus up to 25% in a screened blunt trauma population.16 Computed tomographic angiography has been accepted as the screening modality for blunt cervical vascular
injury, as it compares favorably with conventional angiography.17 The majority of blunt cervical vascular injuries only requires medical treatment with either antiplatelet or anticoagulation therapy for 3 to 6 months, but the optimal agent is unknown because there are no randomized controlled study comparing the two.18 Recent meta-analyses showed no difference between antiplatelet agents and warfarin.19,20 Indications for invasive therapy include progression of neurologic symptoms, persistence of pseudoaneurysm despite antithrombotic treatment, and worsening chronic dissection. The choice of therapy, endovascular or open, is dependent on location of injury, contraindication to antithrombotic therapy, and compliance with follow-up. Surgical repair can usually be done primarily or with patch angioplasty. Vertebral artery injury is a rare occurrence, with an incidence of up to 0.77% of all trauma admissions. Medical treatment for blunt injuries with antithrombotic agents is identical to treatment for carotid artery injury. In fact, most case series describe both carotid and vertebral artery injuries simultaneously.20 Exposure of the vertebral artery depends on the particular segment injured. The most accessible segment is the first segment (V1), which begins at the origin and ends at C6. Exposure requires dividing the sternocleidomastoid and anterior scalene muscle from their thoracic outlet attachments. The phrenic nerve is at risk in this area. The second segment (V2) travels through C6 to C2 transverse foramens and requires resection of the anterior transverse process. This dissection is hazardous because of the adjacent nerve roots and an extensive venous network. In addition, the artery in this segment is deficient in the external elastic lamina and fragile. The third segment (V3) begins at C2 and travels to the skull base. Exposure requires extending the cervical incision posteriorly to the mastoid process. The sternocleidomastoid muscle is divided with care not to injure the spinal accessory nerve. The lateral process of C1 also needs to be resected to gain access to the V3. The fourth segment (V4) is intracranial, as it travels along the brainstem to join the contralateral vertebral artery. Because of these difficult and hazardous exposures, surgical treatment of vertebral artery hemorrhage is best treated with ligation at V1. Continued bleeding from the other segments can be temporarily treated with bone wax packings or balloon occlusive devices before definitive endoluminal embolization at the distal end of the vessel.21
Table 3 Exposure Incisions for Cervical and Great Vessels Injury Zone III Posteriorly to mastoid process with subluxation of mandible Cervical (anterior border of SCM) Supraclavicular Infraclavicular Median sternotomy 2nd or 3rd ICS left anterolateral thoracotomy
Zone I
Proximal Subclavian
ⴙ
ⴙ/ⴚ ⴙ/ⴚ
ⴙ/ⴚ ⴙ/ⴚ (left subclavian)
ⴙ/ⴚ
ⴙ
ⴙ (right subclavian) ⴙ (left subclavian)
Zone II
Distal Subclavian
Axillary
ⴙ ⴙ/ⴚ
ⴙ/ⴚ ⴙ
ⴙ ⴙ
Abbreviations: ICS, intercostal space; SCM, sternocleidomastoid muscle.
Management of civilian and military vascular trauma
Axillosubclavian Injuries Injury to the subclavian vessels has a high morbidity and mortality. Demetriades et al documented a 61% prehospital and 15.5% perioperative mortality rate in their series of 228 penetrating subclavian vessel injuries.22 Surgical dissection in the thoracic outlet region is highly morbid due to the adjacent brachial plexus, surrounding hematoma, and associated pulmonary and mediastinal injuries of these traumatic injuries. Therefore, it is usually necessary for hemodynamically unstable patients only. In stable patients, it is prudent to obtain imaging before therapy, usually with computed tomographic angiography. This allows evaluation of associated cervical, thoracic, and mediastinal injuries. But the “gold standard” is conventional angiography because of its potential for diagnosis and therapy. Because of the morbidity concerns of surgical treatment, endovascular treatment has evolved into the ideal therapy in the hemodynamically stable patient. Even if surgical repair is indicated, a large compliant occlusion balloon can be placed at the time of angiography for proximal control. If indicated in an unstable patient, the subclavian artery can be ligated without resulting in severe ischemia due to the abundance of collaterals. If limiting claudication occurs the artery can be reconstructed electively.23-25 Exposure of the right subclavian artery or innominate artery for proximal control is through a median sternotomy. The proximal left subclavian artery is accessed with a high anterolateral thoracotomy in the second or third intercostal space. The clavicle can be resected as needed. Distal subclavian exposure requires a supraclavicular incision. Isolated axillary artery injury can be treated with an infraclavicular incision, but proximal control usually requires exposure of the subclavian artery (Table 3).
Aortic and Caval Injuries Aortic injury (predominantly located at the isthmus) is the second most common cause of death in blunt trauma.26 Parmley et al advocated urgent surgery in this patient population as they had a 61% 7-day mortality rate in their series.27 The treatment paradigm has shifted since then to a nonoperative approach in hemodynamically stable patients, with several studies showing no increase in survival with early surgery.28-30 Blood pressure control should be the initial treatment goal. Simon and Leslie identified several risk factors for failure of conservative management: increasing mediastinal hematoma or pleural effusion, extravasation of contrast, malperfusion complications, and hypotension.31 Surgical repair of the descending thoracic aorta requires a left thoracotomy. After obtaining proximal and distal control, repair of injury is standard with primary or, more often, interposition graft repair. Distal aortic perfusion during aortic clamping is usually required and can be via a left atrial to distal aorta, right atrium to femoral artery, or femoral artery to femoral vein bypass. Repair of the great vessels can be performed with interposition grafts via side-biting vascular clamps without the need for cardiopulmonary bypass. Exposures were described in earlier sections.
239 The vascular abdomen is divided into three retroperitoneal zones. Zone I is the midline and includes the supramesocolic vasculature (celiac trunk, superior mesenteric artery, renal arteries, inferior vena cava (IVC) and its branches, suprarenal aorta) and the inframesocolic vasculatures (inferior mesenteric artery, IVC, infrarenal aorta). Zone II is the perinephric regions. Zone III is the pelvic region and includes the iliac vessels. Management of abdominal vascular trauma depends on the type and location of injury. Exposure of the supramesocolic Zone I entails mobilization and medial rotation the left colon, spleen, tail of pancreas, stomach, and possibly left kidney. This will gain exposure to the aorta, celiac, superior mesenteric artery, and left renal artery. Mobilization and medial rotation of the right colon, duodenum, and head of pancreas will expose the right renal artery and supramesocolic IVC. The inframesocolic Zone I is exposed by retracting the mesocolon cephalad and small bowel to the right and dividing the parietal peritoneum overlying the aorta or IVC. Mobilization and medial rotation of the right colon, duodenum, and head of pancreas or left colon will also gain access to the right and left Zone II, respectively. Medial rotation of the right or left colon will also allow exposure of Zone III inferiorly. Surgical treatment of the specific vessel injury follows the basic principles of vascular surgery. Primary repair can be done with lateral arteriorraphy or end-to-end anastomosis, if possible. If reconstruction is required, then autogenous vein or polytetraflouroethylene are both optional conduits. In the setting of enteric contamination, it is not desirable but permissible in life-saving situations to use polytetraflouroethylene, but copious irrigation and vascularized tissue coverage of the anastomosis is imperative.32 Ligation of the celiac trunk (or its branches) or the inferior mesenteric artery is usually benign. On the other hand, ligation of the superior mesenteric artery has significant risk of extensive bowel ischemia. Zone II hematoma in blunt trauma should not be explored unless it is expanding. On the contrary, all penetrating trauma Zone II hematomas should be explored. Treatment options include nonoperative, revascularization, or nephrectomy. Revascularization of occluded renal arteries should not be attempted unless ischemia time is less than 6 hours, there are bilateral renal injuries, or there is injury to a solitary kidney.33-35 Zone III hematomas should be explored if due to a penetrating injury, or to a blunt injury with a resulting expanding hematoma or an abnormal femoral pulse. Ligation of common or external iliac is not tolerable and should not be done. In damage-control situations, intraluminal shunting is advisable. As with extremity vascular injuries, development of compartment syndrome is possible and patients should be monitored; and there should be a low threshold for fasciotomy. Vena caval injury can usually be repaired primarily with lateral venorrhaphy, but patch angioplasty and polytetraflouroethylene interposition graft may be necessary for larger injuries. The key is to avoid a subsequent stenosis after the repair, which is at risk of developing thrombosis or embolism; a temporary IVC filter may be required in such a case.
240 Ligation of the infrarenal IVC may be tolerated and necessary in unstable patients, but all suprarenal IVC injuries must be repaired due to the frequent occurrence of hemodynamic instability secondary to drop in preload and significant risk of renal failure with ligation at this level.36 Exposure of the retrohepatic vena cava is very difficult. A retrohepatic hematoma is the only exception to mandatory exploration of all penetrating trauma hematoma. Perihepatic packing is the first-line treatment, and can be left in place for 24 to 48 hours before a second-look operation. If all else fails, then atriocaval shunting, total hepatic vascular isolation, or division of the liver to gain exposure can be attempted for hemorrhage control.
Iatrogenic Injury Iatrogenic vascular injury is an increasing problem, comprising up to 33% of the current civilian vascular trauma patient population.37,38 The rise of iatrogenic vascular injury results from more frequent catheter-based therapies. Of these, 60% are due to femoral access complications and 27% are intraoperative injuries.4 Aside from percutaneous access complications, these injuries are also associated with orthopedic and spine procedures.39 Wood et al40 systematically reviewed 40 articles that reported the frequency of vascular injury with anterior lumbosacral spine surgery. The overall vascular complication rate was 5% (range, 0 to 18%), and venous injury was more common than arterial injury (up to 18% v 5%). The most common vessels injured were the left common iliac vein, IVC, and iliolumbar vein, usually due to retraction of the vessels. Procedural risk factors were L4-L5 exposure, revision surgery, transperitoneal approach, and laparoscopic technique. The authors recommended having a vascular surgeon available when these risk factors were present.40 More of these iatrogenic injuries are requiring invasive therapy to either treat or prevent complications. Guilbert et al41 reported a case series of 13 patients who had either carotid or subclavian artery cannulation with ⱖ7Fr catheter during internal jugular vein central line placements. Five patients were treated with a “pull and pressure” method of manual compression. All had subsequent complications of bleeding, stroke, or death. Eight patients, on the other hand, were treated with either open repair or an endovascular approach of catheter removal, and none had complications. They performed a meta-analysis comprising 30 patients with internal jugular vein line misplacement. Seventeen patients were treated with the pull/pressure method, and 13 patients were treated with open or endovascular repair. All eight patients who developed complications (airway compromise due to hematoma, pseudoaneurysm, hemothorax, and death) were from the pull/pressure group.41
War and Vascular Trauma The first recorded attempts at repair of arterial injuries were during World War I by Croatian surgeons, but the techniques used remain unknown. Long evacuation times for casualties, sepsis, and poor instruments also limited interest
T. Nguyen, J. Kalish, and J. Woodson and feasibility of repairing injured vessels. Debakey and Simeone reviewed the results of 2,471 vascular injuries resulting from World War II and documented a 50% amputation rate when ligation of injured vessels was performed.42 Despite this appalling high rate of amputation, they still concluded that arterial repair was not warranted in most cases because of the high complication rates secondary to sepsis and thrombosis. The Korean conflict was marked by the US Army Fielding Mobile Army Surgical Hospitals (MASH units) and surgical research teams. Casualty evacuation times were improved with the use of helicopters, and antibiotics were more plentiful than in previous wars. These conditions permitted special surgical teams to explore the potential repair of vascular injuries and document a decline in extremity amputation rate from the 50% seen in World War II to 13% when vascular injuries were repaired. The Vietnam War marked advances in the utilization of helicopters for transporting troops and wounded soldiers. Combat medics were better trained to control hemorrhage and specialized centers were identified by the US Army to treat and evaluate vascular injuries. Colonel Norman Rich established the Vietnam Vascular Registry at Walter Reed Army Hospital. This registry helped define the optimal algorithms for managing patients with vascular trauma, such as the importance of repairing a venous injury occurring concomitantly with a popliteal artery injury to improve patency rates of the arterial repair. As previously stated, the advancement in management of vascular trauma has been written in the history of the wars of the past century. At the time of the writing of this article, America has been at war for a decade and old lessons about the management of vascular trauma have been reinforced and new lessons have been learned. The wars in Afghanistan (Operation Enduring Freedom) and Iraq (Operation Iraqi Freedom) have been marked by advances in technology, tactical and strategic evacuation (flying intensive care units), and application of body armor. The US Army has developed and fielded a new advanced combat action tourniquet, resuscitation protocols, smaller (20-person) and more mobile trauma resuscitation teams (Forward Surgical Teams), and a Joint Theater Trauma Registry that allows rapid improvement in care. In addition, there has been improvement in the training of medics, surgeons, and trauma teams. All of these improvements have contributed to the lowest case fatality rates in the history of modern warfare. A soldier injured in battle has a ⬎97% chance of surviving if they make it to a Forward Surgical Team. A standard has been set in the combat zone that all injured soldiers will receive Trauma Center Level care within the first “golden hour” defined by civilian trauma systems. The signature injury-producing weapon of Operation Iraqi Freedom and Operation Enduring Freedom is the improvised explosive device. Improvement in protective body and vehicle armor has contributed to soldier survivability, but the rate of extremity trauma is now higher in survivors than previously reported in earlier wars. Extremity injury now accounts for 40% to 70% of all combat wounds, with 70% of
Management of civilian and military vascular trauma extremity injuries occurring on the lower extremities. Vascular injuries occur in 5% to 7% of all those injured on the battlefield. Clouse et al reviewed the current status of vascular trauma in wartime using the Balad Vascular Registry from Iraq.43 They noted that cervical vascular injuries accounted for 16% of vascular trauma, with carotid injuries constituting nearly three-quarters (73%) of this group. They also reported an increased use of temporary vascular shunts to perfuse limbs, while other priorities were addressed or while patients were transported to a higher level of care. Eighty-six percent of shunts remained patent during their period of use without anticoagulants. Extensive soft-tissue and bony injuries (reflected in a high Mangled Extremity Severity Score) were the primary reasons for limb loss, rather than inability to revascularize the limb. The management strategy of rapid evacuation, temporary shunting, and early definitive vascular repair in the combat zone has resulted in excellent limb-salvage rates. The recent wars have produced only a limited experience with endovascular management of vascular trauma. Isolated subclavian artery and carotid-jugular fistula repairs with stent grafts have been reported. The long logistical trail, varying endovascular abilities of surgeons, and multiple injuries of victims have limited the application of endovascular techniques. These issues are now being analyzed. The ability to rapidly evacuate critically ill soldiers from the combat zone using Critical Care Air Transport Teams within hours to days after wounding increases the possibility of applying endovascular therapies at medical centers remote from the battlefield. There have been ⬎30,000 casualties, with only 1,200 amputations resulting from Operation Iraqi Freedom and Operation Enduring Freedom. Limb salvage revascularization surgery, coupled with superb rehabilitation programs, has returned hundreds of soldiers and civilians injured on the battlefield to productive lives. If war is the dark side of humanity, then the advances in medical care resulting from this experience represent the hope for humanity.
Conclusions The tenets of management of vascular trauma have evolved from the many lessons that can be traced through different time periods, different wars, and different battlefields across the world. Vascular surgical care will always rely on the basic premise of “stopping the bleeding,” and restoring perfusion. Although open surgical management has always been the gold standard for dealing with vascular trauma, the use of endovascular techniques is becoming more prominent for selected indications. The benefits and detriments of these newer technologies will require constant reevaluation to arrive at the optimal care algorithms as the future unfolds.
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