Ischemic injury

There is a differential degree of tissue ischemia tolerance for various organs that is dependent on each tissue’s baseline metabolic demand. Critical ischemia of human skeletal muscle under normothermic conditions is more than 2 hours, whereas jejunum develops histological changes after approximately 30 minutes of ischemia. Decreased oxygen delivery to tissue results in decreased mitochondrial energy production (adenosine triphosphate [ATP] synthesis, oxidative phosphorylation) and a marked decrease in cellular energy stores (ATP content). Inadequate energy stores result in disturbances of cellular ion homeostasis, activation of hydrolases, and increases in permeability of cellular membranes. As ischemia progresses, there is a logarithmic increase in adverse ion homeostasis and activation of hydrolases. As ATP is degraded, cellular lysosomes leak hydrogen ions, and cells increase their glycolytic rate, resulting in cellular acidosis. Acidosis impairs the function of Na⁺/K⁺-ATPase and other enzymes responsible for managing cellular ion homeostasis, resulting in increased cytosolic Na⁺ and Ca²⁺ concentrations. Increased levels of Ca²⁺ concentration activate phospholipases (especially phospholipase A₂) and proteases (calpains), which enhance tissue injury. Activated phospholipases and calpains respectively degrade membrane phospholipid moieties and cytoskeletal proteins to exacerbate tissue injury.

Key events occur during ischemia that set the stage for worsening injury during reperfusion. One of these is the conversion of xanthine dehydrogenase (D) to xanthine oxidase (O). Xanthine dehydrogenase uses NAD⁺ as an electron acceptor during the oxidation of xanthine and hypoxanthine. Heat, proteolysis, and reducing agents such as sulfhydryl compounds can transform the D to the O form, which is incapable of using NAD+ as an electron acceptor. The O form uses oxygen as an electron acceptor, and generates superoxide anion and hydrogen peroxide during the oxidation of hypoxanthine and xanthine. Some investigators have proposed that calcium mediated activation of proteases converts the dehydrogenase form to the oxidase form.

Reperfusion injury

There are metabolic, thrombotic, and inflammatory components of reperfusion injury. The degree to which reperfusion either restores tissue integrity or exacerbates ischemic injury is dependent primarily on the duration of ischemia. It is indeed paradoxical that moderate ischemia followed by reperfusion may cause a more fulminant postischemic tissue injury than ischemia alone. However, without reperfusion, the loss of function in the brain, gut, heart, or limb may have more catastrophic outcome than seen with reperfusion.

Vascular endothelium plays a major role in modulating the tissue response to reperfusion. The generation of reactive oxygen metabolites by calcium-mediated xanthine oxidase–dependent pathways in vascular endothelium during reperfusion contribute to local injury, vascular permeability, and autocrine and paracrine signaling. The increased generation of reactive oxygen metabolites during reperfusion compromises production of nitric oxide (NO) and prostaglandins (PGs), which contributes to alteration of vascular tone. Decreased endothelial ATP levels results in a loss of the apposition of endothelial monolayers, which triggers both an increase in vascular permeability and a decrease in vascular tone.

It is the induction of inflammatory mediator protein synthesis/deposition, decreased vascular tone, and endothelial cell (EC) apposition that leads to the development of the no-reflow phenomenon. A variety of inflammatory mediators are delivered by bloodborne cells (macrophages, lymphocytes, neutrophils, mast cells, platelets) to reperfused tissues. Noncellular elements, such as the complement system, reactive oxygen species (ROS), nitric oxide, and pro- and antiinflammatory cytokines, are also believed to modulate the complex scenario of reperfusion injury. Ischemia/reperfusion injury is believed to manifest clinically as development of cardiac arrhythmias, the evolution of stroke, translocation of bacteria across the bowel wall following revascularization, early organ dysfunction following transplant, and compartment syndrome.

Technique of fasciotomy

A single method of fasciotomy is not universally suitable for all indications. Fasciotomy through limited skin incisions has been both advocated and denounced by many specialists. The rationale for limited skin incisions is based on the concept that the fascia is the limiting constrictive tissue, whereas the skin contributes to the tamponade in certain instances. Limited skin incision fasciotomy is associated with minimal or no morbidity. Infection is less likely, and this technique does not leave large open wounds that can be troublesome in the setting of anticoagulant therapy. In the performance of limited fasciotomy, the skin is not incised along the length of the extremity. By two or three short vertical incisions, the investing fascia can be identified and incised. Long skin incisions are necessary when there is massive swelling and when, on clinical examination, the skin contributes to the constrictive process. The incisions are planned such that vascular or nerve repairs are not exposed. In the posterior medial long incision, it is necessary to release the deep compartment by retracting the gastrocnemius and soleus muscles. In the anterolateral incision, the investing fascia is incised, and the extensor digitorum and peroneal muscles are separated where the deep peroneal nerve can be seen. In the upper extremities, the incisions are made from just proximal to the wrist to the elbow.

Thoracic aorta

Traumatic aortic rupture is a devastating clinical problem that is difficult to manage owing to the need to approach aortic repair in concert with management of complex associated injuries to nonvascular organ systems (Fig. 61-1). The natural history of aortic transection is relatively self-selective, with a significant majority of patients exsanguinating at the scene. Of those who make it to the hospital alive, upwards of 38% die largely as a result of associated injuries.¹² Fabian et al. estimate the incidence of traumatic aortic disruptions in the United States to be between 7500 and 8000 patients annually; about 1000 to 1500 of these patients arrive at hospitals alive.¹³ It took 50 centers 2.5 years to generate 274 patients for this prospective report. This averages just over two patients per year per center. Despite the low volume, contemporary analysis reveals that of the 9% to 19% who reach the hospital alive,¹⁴ approximately 30% will die within the next 6 hours, and a total of 50% within 24 hours.¹⁵

Figure 61-1 Thoracic aortic injury and associated nonvascular injuries.

Spiral thoracic computed tomography (CT) image demonstrating aortic transection 2 cm distal (circled) to subclavian artery origin, with surrounding traumatic thoracic pseudoaneurysm and an intraparenchymal tear of right lung (arrow).

Until recently, open operative intervention for these traumatic injuries required thoracotomy, anticoagulation, and application of an aortic cross-clamp. These operative maneuvers conceded the potential of exacerbating associated injuries and spinal cord injury.^13,16,17 Proximal-to-distal aortic bypass using a Gott Shunt, left heart bypass with heparin-bonded circuits, and cardiopulmonary bypass (CPB) may all significantly reduce the likelihood of paraplegia.^18,19 Thus, the current status of traumatic aortic disruption and traditional repair is not ideal. Advances in endovascular repair techniques for traumatic rupture have resulted in a major change in the approach to treatment of this devastating clinical entity.^20–22 This change in approach is based on and supported by improved mortality associated with repair by endovascular vs. open techniques in patients with multiple trauma²³ (Fig. 61-2).

Figure 61-2 Thoracic aortic disruption.

A, Thoracic aortogram illustrating a 4-cm pseudoaneurysm (circled) in descending thoracic aorta, 2 cm from subclavian artery. B, Post-deployment aortogram revealing no endoleak or extravasation.

Thoracic venae cavae

The superior vena cava is formed by the confluence of the left and right brachiocephalic veins in the superior mediastinum at the level of the right first costal cartilage. It descends down 5 to 7 cm to where it enters the posterior aspect of the right atrium at the level of the third costochondral cartilage. The inferior vena cava (IVC) enters the chest at the level of T8 and has a short posterior course to the right atrium. Because of the location and short segments of these structures, the intrathoracic venae cavae rarely suffer traumatic injury. The low-pressure system and distendabilty of the vessels make blunt trauma a rare etiology of injury. Penetrating injury to the chest or iatrogenic injury are more common etiologies. Cardiac tamponade can be a frequent presentation following injury to the thoracic venae cavae, owing to the pericardium’s extension and envelopment of the proximal portions of the vessels prior to entering the heart.

Simple isolated injuries to the thoracic venae cavae can be managed with lateral venorrhaphy. Partial-occluding clamps or temporary inflow occlusion can be used in these circumstances to facilitate repair.³⁰ Complex injuries to the venae cavae or associated injuries to the heart may require CPB and/or interposition grafts for exposure and repair.

Pulmonary vessels

Trauma to the main right or left pulmonary arteries is extremely rare and almost exclusively found after penetrating traumatic injury. Some case reports have described blunt traumatic injury to the main pulmonary arteries, but it remains exceedingly rare.³¹ As with many of the great vessel injuries, cardiac tamponade or hemopericardium is the common presenting finding. Usually the diagnosis is made in the operating room during an empirical thoracotomy for hemopericardium. Distal pulmonary vascular injuries beyond the mediastinum can be seen following both blunt and penetrating trauma. Extensive vascular injury or significant injury to the hilar region may necessitate a pneumonectomy, which bears a significantly high mortality rate in trauma situations.³²

Diagnostic evaluation

With penetrating injuries to the neck, the depth, location, and presence or absence of hard/soft signs of vascular trauma dictate the progression and trajectory of care. If the platysma muscle has not been violated by the penetrating insult, no immediate operative exploration is warranted. The presence of soft vascular injury signs in this scenario may necessitate further diagnostic imaging to rule out occult injury. If the injury traverses the platysma and/or hard signs of vascular injury are present, operative intervention or diagnostic interrogation (e.g., CTA) should not be delayed.

Anatomical considerations

The neck is divided anatomically into three zones of injury (Box 61-2). Zone I comprises the area from the thoracic outlet (the level of jugular notch) to the cricoid cartilage, zone II begins at level of the cricoid cartilage and terminates at the angle of the mandible, and zone III extends from the angle of the mandible to the skull base. The zone divisions were based on the anatomical relationships of the neurovascular and aerodigestive tract structures, as well as the surgical approach for exposure.

Operative approach/open surgical management

Surgical exposure of the neck differs markedly depending on the zone of injury. Exposure of a zone II injury is straightforward and typically accomplished through a standard oblique incision along the anterior border of the sternocleidomastoid. This affords appropriate exposure and easy accessibility to the carotid sheath and its neurovascular contents.

The surgical approaches for zone I and III injuries can be significantly more complicated and challenging. To obtain adequate proximal vascular control and exposure, vascular injuries within zone I frequently require a median sternotomy or supraclavicular “trap-door” incision in addition to the standard cervical oblique incision. Zone III injuries may necessitate cephalad extension of the exposure to attain distal vascular control. Maneuvers such as dislocation or partial resection of the mandible are not infrequent, especially in high zone III injuries. Temporary control of bleeding at or near the skull base can be accomplished through insertion and inflation of a Fogarty catheter into the injured vessel.³⁸

Endovascular management

Though endovascular management is less prevalent in blunt carotid injury, it has provided some promising results in the management of penetrating carotid trauma, especially in zone I and high zone III (internal carotid artery [ICA]) injuries.^39,40 Traditionally, ICA injuries (pseudoaneurysm and dissections), albeit rare, warrant anatomical reconstruction to prevent devastating ischemic neurological insults. Operating high in the neck is technically demanding and can be associated with cranial nerve injury; thus, endovascular stenting and coiling has the potential to limit iatrogenic damage associated with open exploration. Recent reviews have demonstrated that stent graft placement for traumatic ICA pseudoaneurysms have been successful in neurologically symptomatic patients following trauma.^41,42 Consideration must be given to thromboembolic events associated with stent graft placement, the potential for intimal hyperplasia formation, and restenosis. The anatomical tortuosity of the vessel may prevent safe crossing of the traumatic lesion with a guidewire. A recent retrospective review of 113 patients with blunt or penetrating carotid injury demonstrated a promising short-term patency (up to 2 years) of carotid stent grafts (80%).⁴³

Diagnostic evaluation

In most emergency situations, multidetector CTA remains the initial tool for evaluation of carotid injuries because it can often be performed expeditiously near or in the emergency room. Adequacy of the older single-slice helical CTA in diagnosing BCVI was limited by sensitivities and specificities of 68% and 67%, respectively.⁴⁸ However, several studies have shown the effectiveness of 16-channel multislice CTA in diagnosis of BCVI,^44,49 with sensitivities and specificities each greater than 94%. The somewhat subtle nature of blunt carotid injury makes digital subtraction angiography (DSA) the gold standard for the diagnosis of blunt carotid injury. Imaging by CTA may be compromised in situations where metallic artifact is present (shrapnel, plates, prosthesis, etc.). Although DSA is an invasive method, it not only depicts the extent and severity of vessel injury, it can also provide information about the integrity of cerebral circulation. Magnetic resonance angiography is another safe, noninvasive technique that can provide data concerning vessel morphology and blood flow. Its accuracy in diagnosing BCVI may rival that of CTA, but time required for the examination, difficulty monitoring the patient during the study, and high cost limit its use.⁴⁵ Duplex ultrasonography is used more in penetrating carotid trauma but is not sensitive enough to be the screening modality of choice in BCVI.⁴⁴

Classification of blunt carotid injury: the Denver scale

The Denver Scale (Table 61-2) has been widely accepted and used to classify blunt carotid injury.⁵⁰ It was employed to standardize and direct care for the different grades of vessel injury based on multiplanar CTA or DSA findings. Grade I to IV injuries typically warrant anticoagulation as the mainstay of treatment, with consideration of surgical intervention if contraindication of anticoagulation or further neurological deterioration exists. Grade V injury, which represents complete transection with extravasation, is most appropriately treated through surgical intervention, whether it be an endovascular or open approach.

^{Table 61-2} Denver Scale for Blunt Carotid Injury

From Biffl WL, Moore EE, Offner PJ, et al: Blunt carotid arterial injuries: Implications of a new grading scale. J Trauma 47:845–853, 1999.

Clinical management

Despite increased awareness of blunt carotid injury, there is no agreement on the best therapeutic approach. Accumulated data suggest that conservative therapy using antithrombotic therapy with heparin prevents cerebral infarction. Similarly, antiplatelet therapy and anticoagulation with warfarin (international normalized ratio [INR] 2-3) were equally effective in reducing risk of stroke following BCVI.^45,51 In a recent analysis of the national trauma database, a comparison of functional independence following BCVI in patients treated conservatively (anticoagulation and/or antiplatelet agents) vs. operatively (open and endovascular treatment) was performed.⁵² There was no difference in functional outcome in these patients, regardless of conservative or operative intervention. The only demographic difference among the groups was greater injury severity score in patients undergoing endovascular repair. In most studies, BCVI in surgically accessible areas are treated operatively; however, the vast majority of BCVI lesions occur in surgically challenging areas high within the carotid canal or foramen transversarium. Such locations make standard operative approaches for thrombectomy or reconstruction difficult.⁵³

Retroperitoneal hematomas

Retroperitoneal hematomas occur in more than 90% of abdominal vascular injuries.⁵⁹ The retroperitoneum is divided into three main zones of injury: zone I is the central/midline retroperitoneum, zone II encompasses the perinephric space, and zone III comprises the pelvic retroperitoneum. Treatment of retroperitoneal hematomas varies depending on the anatomical location and mechanism of injury.

Zone I injuries mandate exploration for both penetrating and blunt injury because of the major vascular structures residing in this region and the unforgiving consequences if injury diagnosis is delayed. The transverse mesocolon subdivides this zone into the central supra- and infra-mesocolic spaces. Hematomas in the central supramesocolic space develop behind the lesser omentum and push the stomach forward. These hematomas result from injury to the suprarenal aorta, celiac axis, proximal superior mesenteric artery (SMA), or proximal renal arteries. Thus, for surgical exploration, proximal control of the aorta should be obtained at the level of the diaphragm, and exposure carried out with a left-sided medial visceral rotation (Mattox maneuver). Central infra-mesocolic hematomas present behind the root of the small-bowel mesentery are a consequence of either infrarenal aorta or IVC injury. Exposure is obtained through a retroperitoneal opening on the midline, and control of the aorta is gained above the celiac axis.

Zone II retroperitoneal hematomas are commonly due to injury to the renal vasculature or parenchyma. All zone II hematomas secondary to penetrating trauma necessitate operative exploration because of the risk for vascular laceration. Stable zone II hematomas following blunt trauma are best managed conservatively because exploration entails opening the Gerota fascia, which under these conditions bears a high likelihood of causing further injury to an already damaged kidney.

Pelvic retroperitoneal hematomas, or zone III hematomas, are typically managed nonoperatively. Iliac vessel injury or suspicion of it represents the only true indication for surgical exploration. This is more common following penetrating injury to the pelvis, as opposed to those of blunt mechanisms. Hematomas arising from blunt means typically result from pelvic fractures, where external fixation and angiographic coil embolization represent the best treatment modalities.

Abdominal aorta

The aorta is the largest artery in the body, and its abdominal portion spans from where it traverses the diaphragm at the level of T12 to where it bifurcates into the iliac arteries at the L4/L5 level. It is the most commonly injured artery in the abdomen following trauma; many times, aortic injury presents as a lethal condition. Blunt injury to the abdominal aorta is most often associated with motor vehicle accidents, followed by falls and direct blows to the abdomen. The mortality associated with blunt aortic injury is estimated to be around 30%.^56,68 Penetrating trauma remains the most common method of injury to the abdominal aorta and carries a significantly higher mortality than blunt injury. Mortality following penetrating injury (e.g., fire arm blasts, knife stab wounds, etc.), has been estimated to be between 67% and 85%.⁶⁹

Many patients with significant aortic injury never make it to the hospital. The fortunate few who make it to a medical care facility present with injuries such as intimal disruptions, thrombosis, and/or contained retroperitoneal hematomas.^{54,55,59,63,70} The clinical presentation will depend on the mechanism of trauma, type of aortic injury, prehospital time, and associated traumatic vascular and nonvascular injuries. Penetrating injuries typically present in a dramatic fashion with profound hypotension, shock, and hemodynamic collapse. Under certain conditions, an emergency resuscitative thoracotomy can temporize cardiovascular collapse in order to get the patient to the operating room for definitive surgical intention.

Ultrasonography during the FAST exam can immediately inform the trauma team of the presence of free intraperitoneal fluid and, in the setting of hemodynamic instability, the affirmative need for operative intervention. Blunt injuries tend to have a less dramatic presentation with normotensive patients but can still have significant injury leading to visceral, renal, or lower-extremity ischemia. Multidetector CT scans provide a fast, accurate method of evaluating aortic injuries in hemodynamically stable patients. The diagnosis in unstable patients should be made during laparotomy. Depending on the findings from clinical examination and imaging studies, endovascular techniques can be implemented to treat both penetrating and blunt acute traumatic injuries.^3,71–74

The significantly high incidence of associated injuries following penetrating abdominal trauma (>90%)⁷⁵ make open surgical intervention the gold standard for repair, in part because assessing and treating bowel and solid-organ injuries are critical. When the abdomen is explored, all four quadrants should be packed off, then examination of the quadrants should be done meticulously to identify all injuries, vascular and nonvascular alike. For supramesocolic zone I injuries, proximal control is obtained by clamping or compressing the aorta as it traverses the diaphragm. If the injury to the aorta resides high on the abdominal aorta, proximal control can be gained above the diaphragm through a left thoracotomy. The injured portion of the aorta or associated injured vessels can be exposed by means of a left-sided medial visceral rotation (Mattox maneuver). Infra-mesocolic zone I hematomas result from injury to either the infrarenal aorta or IVC. In this scenario, proximal control is gained at the supraceliac aorta, and exposure is provided by opening the posterior peritoneum in the midline.

Endovascular management is becoming far more frequently used with aortic trauma, and is more common following blunt injury than penetrating injury.^3,73,74 Much of the impetus for its use in trauma has been drawn from the success of stent grafting in the treatment of nontraumatic aortic disease (e.g., aneurysms, ruptures, dissections, fistula formations, thrombosis). The extension of endovascular techniques into the setting of trauma is logical and has provided more treatment options for patients presenting with contained retroperitoneal hematomas.⁷³ If a patient has a perforated viscous, small-bowel anastomosis, partial colectomy, or ostomy, endoluminal treatment of associated arterial injuries avoids opening the retroperitoneum and placing a prosthetic conduit in a contaminated field.

Celiac axis injury

Celiac artery injuries are rare and almost always a result of penetrating trauma. In a review of 302 patients with abdominal vascular injuries, the celiac artery was injured in only 3.3% of cases.⁵⁹ The celiac axis gives rise to the left gastric, splenic, and common hepatic arteries. Injuries amenable to primary repair should be carried out, but ligation of the artery can be done without ischemic sequelae because of the robust collateral circulation of the proximal gastrointestinal tract. That being said, endovascular coiling and embolization is a frequently used technique for controlling hemorrhage from the hepatic and splenic vasculature following blunt trauma.⁷⁶ The mortality rate for celiac axis injuries has been reported to range between 38% and 75%.⁵⁶ However, many of these patients have associated vascular injuries that contribute to the high mortality rate; isolated celiac injury likely carries a much lower mortality rate.

Superior mesenteric artery and vein injury

Superior mesenteric artery injury presents as either free intraperitoneal hemorrhage, a central (zone I) supramesocolic retroperitoneal hematoma, ischemic proximal small bowel, or any combination of the three. Superior mesenteric artery injuries account for roughly 10% of all abdominal vascular injuries⁵⁹ and are diagnosed in less than 0.1% of total trauma admissions.⁷⁷ It is the second most commonly injured abdominal vascular structure following blunt trauma, but penetrating trauma accounts for the significant majority of SMA injuries.⁷⁷ The mortality rate associated with SMA injury is estimated to be as high as 47% to 67%.^54,56,59,77

The SMA is divided into four anatomical zones of injury, which were first described by Fullen et al.,⁷⁸ who also correlated grade of ischemia with injury location (Table 61-4). The affected zone, ischemic grade, and AAST-OIS for abdominal vascular trauma correlate well with mortality.^77,79 The surgical approach is driven by the location of the injury. Injuries to the first two zones should undergo primary repair whenever possible. Ligation of the artery at these levels would result in significant small-bowel ischemia and a poor prognosis without revascularization. Revascularization with autogenous or prosthetic conduits is another option and sometimes necessitates extra-anatomical routes. Zone III and IV injuries should be primarily repaired as well. Should ligation at these levels or of the segmental branches prove necessary for hemostasis, only local ischemia to the small bowel will follow, which segmental bowel resection can remedy. A second-look laparotomy is mandatory to asses the viability and integrity of the small bowel following any surgical manipulation of the SMA. Endovascular techniques have been implemented in limited cases but have demonstrated promise.⁸⁰

Superior mesenteric vein (SMV) injuries are infrequent but incur high mortality rates due to the difficulty in obtaining prompt exposure and hemorrhage control, combined with the high incidence of concomitant portal vein injury.⁸¹ Lateral venorrhaphy is the preferred surgical means of repair for an isolated SMV injury. Graft conduits can restore flow, but thrombosis can be a devastating complication. Ligation of the vein is a plausible surgical option, especially in hemodynamically unstable patients,⁸¹ but carries a risk of venous mesenteric ischemia secondary to splanchnic sequestration. Aggressive resuscitation is vital following venous ligation, and a second-look laparotomy is again standard, as with SMA injuries.

Inferior mesenteric artery and vein injury

Injury to the inferior mesenteric artery (IMA) is typically managed by ligation.⁵⁶ In rare cases, collateral circulation to the descending and sigmoid colons and the upper rectum may be inadequate and result in ischemia to these regions of bowel. Again, this is a very rare occurrence because of the rich collateral flow via the marginal artery and its arcade. Ligation of the inferior mesenteric vein is tolerated much better than that of the SMV and can be done with impunity.

Renovascular injuries

Renovascular injury is relatively uncommon following trauma. The kidney itself is injured in only 1.2% of all trauma cases, and vascular injury only accounts for 2.5% to 4% of those cases.⁸² It does, however, represent roughly 16% of all abdominal vascular trauma.⁵⁹ Renovascular injury is more common following blunt as opposed to penetrating trauma, with blunt trauma making up almost 80% of cases.

The clinical presentation is most often subtle with regard to the vascular injury itself, but associated injuries can cause a more concerning clinical picture, frequently taking precedence over the renovascular injuries. Unlike many other vascular injuries, exsanguination from the renal vasculature is uncommon and is usually contained in the retroperitoneum. Flank pain, proteinuria, and hematuria (gross and microscopic) are findings that indicate the presence of renal vascular injury, but are neither always present nor specific for vascular injury itself. Computed tomography is the best first-line imaging modality for renovascular injuries.⁸³ It can illustrate the extent of parenchymal damage and perfusion, along with the morphology of the retroperitoneal hematoma. Angiography coupled with endovascular techniques is frequently needed to confirm and sometimes treat the vascular injuries.

Renal function is diminished significantly following just 3 to 6 hours of ischemic insult. If revascularization is to be done, it should be accomplished within this window, despite a success rate of 28% for renal function preservation.⁸⁴ Revascularization can be done via primary repair, vein patch angioplasty, interposition grafting, or segmental resection with reanastomosis. This is usually performed if the injury is found during operative exploration or when there is bilateral vascular injury in an attempt to preserve some renal function. A nephrectomy is an accepted surgical treatment/option for devastating unilateral renovascular injuries. Studies support that nephrectomy in the setting of major unilateral vascular injury has comparable mortality, posttreatment renal function, transfusion requirements, and level of service as that of repair.^82,85 Renal vein injury can be repaired similarly to the artery. If devastating injury occurs to the left renal vein, ligation is acceptable. Ligation of the left renal vein near its confluence with the IVC can be tolerated because of accessory venous drainage through the left gonadal, left adrenal, and lumbar veins. Attempts to repair the right renal vein should be made, since the absence of adequate venous collateral flow on the right side will lead to a right nephrectomy. Endovascular approaches to manage renovascular trauma have been useful in selected instances of pseudoaneurysm formation, intimal tears, or AVFs.^85–87

Mortality is hard to estimate because of the significant occurrence of major associated injuries that drive the data. Rates of posttraumatic renal failure and hypertension are low and in two studies were estimated to be 6.4% and 4.5%, respectively.^85,88

Iliac vessel injury

Exsanguination from iliac vessel injuries is common and associated with high mortality resulting from refractory hemorrhage and associated injuries.^89–91 Mortality rates range from 25% to 40%, but the incidence of iliac vessel injury represents 10% of all abdominal vascular injuries and less than 2% of all vascular trauma.⁹¹ Gaining surgical control of the bleeding can be challenging, and many of these patients present acidotic, coagulopathic, and hypothermic from extensive blood loss.^90,91 The close proximity and shared course of the iliac veins make combined arteriovenous injuries a frequent occurrence. The small bowel, colon, urinary bladder, and ureters intimately cohabitate the microenvironment of the iliac vessels, and concomitant injury to these structures are the rule rather than the exception. Extent of injury to the surrounding structures and degree of enteric contamination are principal factors that can increase the complexity of management with regard to repair and/or revascularization.

Injury to the iliac artery or suspicion of it is a clear indication for surgery in zone III retroperitoneal injuries. Proximal control is gained at the infra-mesocolic aorta, with distal control gained at the external iliac at the level of the inguinal ligament. The ascending colon is reflected medially via a Kocher or Cattell-Braasch maneuver, exposing the pelvic retroperitoneum. Primary arteriorrhaphy is the preferred method of repair for a simple injury. Reconstruction can also be accomplished with end-to-end anastomosis of autogenous saphenous vein or polytetrafluoroethylene (PTFE) grafts.⁹⁰ It is important to be cognizant of the fact that prosthetic grafts may be problematic in an environment contaminated by associated small-bowel or colon injury. Iliac injuries are amenable to bailout or damage-control procedures in the circumstance of a patient critically ill due to other traumatic injuries, where an extensive operation is too high risk. Temporary shunt insertion, arterial ligation with delayed extra-anatomical reconstruction, or balloon tamponade of venous injury may be employed in this situation. Iliac vein injury can be even more complex with regard to gaining access and control of the vessel. Occasionally, the iliac artery must be divided to allow adequate access to the venous structures, and then reconstructed following venous repair. Concerns of edema and compartment syndrome following prolonged ischemic time or vein ligation merit a low threshold for lower-extremity fasciotomies. Endovascular techniques have shown utility in selected cases of isolated iliac artery injury. Patients with AVFs, pseudoaneurysms, or major intimal tears may benefit from endovascular stenting and/or coiling rather than open exploration^92,93 (Fig. 61-3).

Figure 61-3 Penetrating iliac artery injury.

A, Arteriogram revealed 10-cm right common iliac artery (CIA) aneurysm with iliocaval fistulae following gunshot wound to abdomen. B, Arteriogram following successful deployment and placement of a covered stent.

Inferior vena cava

The IVC is the most commonly injured vessel in the abdomen, accounting for one fourth of abdominal vascular injuries.⁵⁹ About 90% of injuries to the IVC are a result of penetrating trauma, and approximately 18% have associated aortic injury.^94,95 More than half of patients with IVC injuries will die before reaching the hospital. Of those who make it to a medical care facility, more than half are in class III hemorrhagic shock.⁹⁵ The most important prognostic factors following IVC injury are the grade of hemorrhagic shock, anatomical level of IVC injury, and associated vascular injuries.^58,94–96 Supra- and retrohepatic lacerations have the worst prognosis, and their management can be challenging.

Some IVC injuries present with a contained zone I retroperitoneal hematoma, and the patient will remain hemodynamically stable. In this circumstance, a decision for expectant management for lesions in the retro- or suprahepatic vena cava would be reasonable, despite the dogma of zone I retroperitoneal hematoma treatment. There is a considerable degree of difficulty and mortality associated with surgical exploration.^95,96 Surgical exploration for lesions behind the liver may involve combined entry into the chest and abdomen and require extensive mobilization of the liver, atriocaval shunting, total vascular occlusion, or hepatic vascular isolation. In extreme circumstances, direct exposure of the IVC can also be accomplished through division of the liver along the Cantlie line, though it is rarely employed and only if there is already significant injury to the liver.

Infrarenal caval ligation can be an acceptable treatment in a hemodynamically unstable patient with significant associated traumatic injuries. Ligation above the level of the renal veins would lead to fulminant renal failure and is not an appropriate option. Reconstruction with autogenous vein or prosthetic conduits are the most appropriate treatments despite the low success rate due to the extreme condition of the patient. If ligation of the infrarenal IVC is done, the patient’s bilateral lower extremities should be wrapped and elevated to prevent morbid lower-extremity edema. Patients can experience transient edema in the lower extremities following primary repair of the IVC that causes stenosis. Older patients with IVC stenosis following repair are at increased risk for a pulmonary embolus, so some have advocated vena cava filter placement superior to the repair.⁹⁵

Portal vein injury

The portal vein is made up by the confluence of the superior mesenteric and splenic veins behind the neck of the pancreas. It constitutes 80% of the hepatic blood flow and provides 50% of the hepatic oxygen demand. Its injury accounts for 5% of all abdominal vascular injuries.⁵⁹ The vast majority are a result of penetrating trauma (90%) and associated with other vascular injuries 70% to 90% of the time.⁹⁷ Following penetrating injury, patients usually present with hemorrhagic shock and require an emergent laparotomy. Blunt trauma causing a direct blow to the abdomen or severe deceleration forces can injure the portal vein, usually in combination with the SMV.

The operative exposure for these injuries can be extensive, using an extensive right-sided medial visceral rotation of the ascending colon and duodenum. In some circumstances, especially with combined SMV injuries, this exposure may not be adequate, warranting division of the neck of the pancreas to increase exposure. These patients present in such poor condition that complex reconstructions are rarely feasible or advisable. Primary repair, if acquiescent, is the best surgical treatment. Complex reconstructions should only be done in patients with associated hepatic artery injury not amenable to repair. The combined absence of blood flow through the portal vein and hepatic artery is not compatible with life. These situations merit revascularization with autogenous saphenous vein graft.⁹⁷ Ligation is another option that should be considered for devastating retropancreatic injuries. Similar to ligation of the SMV, splanchnic bed sequestration can lead to patchy bowel-wall necrosis. Massive fluid resuscitation should be expected postoperatively. Historical data indicate survival rates between 55% and 85% following ligation.^97–99 The abdomen should be left open and vacuumed packed, with a planned return visit to the operating room in roughly 48 hours. The mortality rate associated with portal vein injuries can be as high as 50% to 72%.^59,98,99

Subclavian-axillary injury

Much of the course of the subclavian/axillary artery and vein are covered by the clavicle and overlying pectoralis musculature, making injury to these structures uncommon. Penetrating trauma accounts for the overwhelming majority of cases.¹⁰¹ Concomitant injury of artery and vein occurs in roughly 20% of cases.¹⁰² Blunt injury to these structures are rare, but clavicle and first rib fractures/dislocations have been associated with blunt vascular injury in multiple studies.^102–104

Minimizing prehospital time is key to successful management of these injuries. Upon presentation, critical ischemia of the upper extremity is uncommon, and a palpable pulse may be present in the extremity owing to the rich collateral circulation around the axillary artery. Uncontained hemorrhage from these injuries can be devastating and result in mortality at the scene. One study demonstrated an overall mortality rate of 39% in a series of 54 consecutive subclavian artery injuries.¹⁰¹ Another review of 79 patients illustrated that more than 20% of patients with subclavian/axillary injuries arrived at a medical care facility with no vital signs or imminent cardiac arrest due to massive hemorrhage.¹⁰²

If a proximal venous injury from a neck or chest wound is suspected, the patient should be placed in the Trendelenburg position to avoid an embolus (based on the Bernoulli principle of fluid dynamics). In the presence of profound hypotension, major hemorrhage, or an ischemic/threatened limb, surgical intervention should not be delayed. In a hemodynamically stable patient, a careful pulse examination of the upper extremities should be coupled with a low index of suspicion for further evaluation with ABI and/or color-flow Doppler studies.

Similar to other types of vascular injury, multidetector CT scanners are a useful modality, especially with penetrating missile injuries. One study demonstrated that multidetector CT scans were helpful in avoiding unnecessary angiography in 85% of cases involving transmediastinal gunshot wounds.¹⁰⁵ Angiography is less used in the diagnostic setting because of the utility and efficacy of color-flow Doppler and CT, but it continues to have a vital role in the therapeutic arena for managing subclavian and axillary injuries.^{3,73,105–107}

The standard incision for a proximal axillary or midsubclavian artery injury extends from the jugular notch along the clavicle and then downward in the deltopectoral groove. This incision can be combined with a median sternotomy to gain exposure for proximal subclavian injuries. A trap-door incision has been described for proximal left subclavian injuries but carries a host of complications that can be avoided with anterolateral thoracotomy.

Endovascular therapy has been used with high success in both blunt and penetrating trauma in selected patients. Those who are hemodynamically stable and found to have traumatic AVFs, false aneurysms, and focal dissections are ideal candidates. It is important to note that lesions in close proximity to the origins of the vertebral and/or right CCAs may preclude safe deployment of an endovascular stent graft without covering the origin. One series reviewed 23 patients who underwent intervention for traumatic subclavian/axillary artery injuries. Patients who met the criteria for and underwent endovascular stenting had shorter operative time, less blood loss, and similar patency rates.¹⁰⁷

Brachial and forearm vessel injury

The incidence of upper-extremity vascular trauma historically represents 30% of vascular trauma. The upper-arm arterial supply is made up by the brachial and deep brachial arteries. The forearm blood supply consists of the radial, ulnar, and interosseous arteries. Penetrating trauma is the most common etiology of injury, and the brachial artery is damaged more than half the time in upper-extremity vascular injuries.¹⁰⁸ The vascular component of upper-extremity trauma per se does not play a large role in overall mortality, compared to associated traumatic injuries. Nerve injury is widely accepted as the most important prognostic factor/indicator of function.¹⁰⁸ Concomitant bone, nerve, or venous injury has been observed to be as high as 73% in some studies.¹⁰⁹

Angiography remains the gold standard for evaluation/diagnosis of upper-extremity injuries, but noninvasive studies provide good utility in the acute setting. Physical examination and duplex ultrasound studies can diagnose most significant injuries but may miss smaller or more subtle injuries. Compared to conventional angiography, small series have shown CTA to approach 95% sensitivity and 98% specificity for upper-extremity vascular lesions.¹⁰⁸ That accuracy, combined with the easy accessibility of CTA, makes it one of the most common modalities used in evaluating these injuries.

Expedient repair of all brachial or forearm arterial injuries is vital. Critical limb ischemia may develop in as short as 4 hours following injury if not repaired.¹⁰⁸ Furthermore, studies of arterial injuries of the upper extremity repaired more than 12 hours after the traumatic insult suggest that only 25% return to normal arm function.¹¹⁰ Isolated injury to the radial or ulnar artery can usually tolerate ligation without subsequent ischemia because of the rich collateral circulation of the forearm and hand. However, it is important to remember that only 80% to 85% of the population has an intact palmer arch. Under these circumstances, the patient will need repair to the ulnar or radial artery to prevent hand ischemia. Although compartment syndrome is less commonly seen in the upper extremity than the lower extremity, a fasciotomy should be considered following any arterial repair in the arm.

Femoral vessels

Femoral vessel injury is among the most common vascular injuries, constituting approximately 70% of all peripheral vascular injuries.¹¹¹ More than 90% of femoral artery injuries result from penetrating trauma, primarily gunshot wounds.¹⁰⁰ Exsanguination does occur following these injuries, but the superficial course of the vessel allows for prehospital control of hemorrhage through direct pressure.

Obvious injury to the femoral vessels warrants transfer to a surgical suite for repair. Control of the external iliac vessels may be obtained before accessing the contents in the femoral triangle. Exposure of the femoral vessels can be gained through a linear incision along the medial edge of the sartorius muscle below the inguinal ligament. Combined vein and arterial injury can prove challenging, with venous bleeding occasionally proving more challenging than that of the arterial circuit. Historically, the most commonly injured extremity veins include the superficial femoral vein (42%), the popliteal vein (23%), and common femoral vein (14%).¹¹² The contralateral limb should be prepared in case autogenous vein grafts are needed for repair of the injured artery or vein.

In the case of small intimal flaps and pseudoaneurysms, observation, nonoperative management, or endovascular techniques (stenting, coiling, etc.) may provide effective therapy. Anticoagulation may not be an option in trauma patients, depending on the associated injuries, but if the decision for observation or nonoperative management is made, reevaluation by invasive (angiography) or noninvasive (ultrasound, CTA, MRA) methods should be performed to confirm convalescence.

Early diagnosis and aggressive management of femoral vessel injury has led to an amputation rate of less than 9%.¹⁰⁰ In contrast to the strategy employed for venous injury in other parts of the body, femoral vein repair is preferred to ligation. If the femoral vein is ligated, early fasciotomy and meticulous monitoring of compartment pressures should be performed.

Calf vessel injuries

The calf vessels include the vascular circuit starting and extending distally from the popliteal fossa. These vessels include the popliteal, anterior and posterior tibial, and peroneal arteries. Popliteal artery injuries represent one of the most challenging of all vascular extremity injuries to manage. The popliteal artery is the second most commonly injured artery in the leg, and more commonly results from penetrating injury. Blunt popliteal injury is most commonly seen following posterior knee dislocations,¹¹³ which can have significant orthopedic and neurological consequences.

The outcome from popliteal injury depends importantly on the mode of injury. Amputation rates may reach as high as 20% to 50% following a high-velocity gun or shotgun blast, which may lead to significant soft-tissue injury and septic sequelae. A recent review of 24 published series demonstrated a much lower amputation rate of 11%, indicating the marked improvement in limb salvage in modern civilian series.^113,114 The rate of associated injury of local neurovascular structures (popliteal vein, tibial nerve, tibial/peroneal arteries, etc.) involved with penetrating popliteal injury ranges from 20% to 38%.^{113,115–117}

The operative approach taken depends on the location of associated injuries. Popliteal vein injuries should be taken very seriously, with repair or reconstruction performed whenever possible. Because of the significant risk of reperfusion injury and venous congestion, a low threshold should be maintained for fasciotomy in the setting of severe popliteal vessel injury associated with prolonged ischemia or combined arterial/venous injury.

Injury to one of the three infrapopliteal arteries rarely results in limb ischemia in the absence of preexisting occlusive disease. In the setting of isolated hemorrhage from one of these vessels, ligation or embolization is an option. However, when the tibioperoneal truck or two or more of the infrapopliteal arteries are injured, repair or revascularization is vital for limb salvage. Nerve, bone, and soft-tissue damage in this region of the body plays a major role in limb salvage. Historical data demonstrate an amputation rate of 54% when associated orthopedic, nerve, and soft-tissue injuries are present.¹¹⁸

Extremity venous injury

The aggressive approach to arterial injury in the extremities has not been matched in the approach to venous repair. Venous ligation may result in thrombosis and venous insufficiency, ultimately leading to significant chronic disability. A balanced approach should include ligation for injury to minor veins, and repair or reconstruction for larger veins when possible.

False aneurysm

Suspicion of an iatrogenic pseudoaneurysm should occur in the setting of a swollen groin, excessive pain at the insertion site, or soft-tissue hematoma at the puncture site. Presence of a bruit and ongoing pulsatile bleeding are highly suggestive of a pseudoaneurysm. Arterial duplex examination has nearly 100% diagnostic accuracy, and if suspicion is present, no hesitation should delay obtaining the examination (also see Chapter 12). The test is simple, quick, and has excellent sensitivity and specificity. Duplex ultrasonography can be performed at any location in the hospital but may be less efficacious in conditions of morbid obesity or when a very large hematoma is present. The location of certain vessels, including the subclavian, profunda femoris, and visceral arteries can make imaging by duplex ultrasound challenging owing to depth of the vessel, overlying bone, or bowel gas. Duplex ultrasound evaluation in the longitudinal and transverse planes is essential to identify the neck, confirm flow outside the artery, and accurately measure the size of the pseudoaneurysm. Typical characteristics seen on duplex ultrasound imaging include swirling of color flow in a mass distinct from the underlying artery, color flow signal through a tract leading to a sac, and to-and-fro Doppler waveform in the pseudoaneurysm neck. The precise definition of the false aneurysm size and neck is one of the most important parameters for determining treatment options. Larger neck and width often correlates directly with larger arterial defects that are generally more refractory to treatment with minimally invasive techniques. In the setting of a significant drop in blood pressure, decreasing hematocrit, or an obese patient, where duplex ultrasound examination is technically difficult, a CT scan with contrast may be useful to confirm the diagnosis of a pseudoaneurysm and exclude the presence of a large retroperitoneal hematoma.

Arteriovenous fistula

Although physical examination alone is not diagnostic for femoral pseudoaneurysm, it can be highly accurate and specific for detecting the presence of an AVF. A to-and-fro holosystolic/diastolic bruit at the puncture site is both diagnostic and pathognomonic for an AVF. In addition, the intensity of the sounds correlates with the size of the fistula. An ultrasound is unlikely to better characterize the extent of arteriovenous flow in the presence of these clinical findings. In the acute setting, femoral AVFs after groin interventions tend to be small in size and have significantly less flow than AVFs constructed for patients requiring hemodialysis. In certain situations, days, months, or years after trauma or a groin intervention, the insidious onset of heart failure, limb swelling, or claudication can be the initial presentation for an AVF.¹²⁰ The diagnosis of an AVF can be made by duplex ultrasound when the characteristic physical findings are not clearly present (also see Chapter 12). There are strict duplex ultrasound criteria for establishing a diagnosis of AVF:

Computed tomography scans do not provide great efficacy in confirming the diagnosis of a femoral AVF, but in patients who have a more central fistula (aortocaval, iliac artery–iliac vein AVF), CT scanning is essential to delineate the arterial location of the connection and adjacent structures.

False aneurysms

In the absence of impending cutaneous necrosis, femoral nerve compression symptoms, and continued bleeding despite local compression, most pseudoaneurysms can be managed conservatively with observation. In a study of femoral aneurysms 3 cm or less in diameter, not associated with severe pain, and in the setting of no systemic anticoagulation, there was an 89% spontaneous thrombosis rate with no complications. The mean time for thrombosis was 23 days, with a mean number of 2.6 duplex examinations per patient.¹²¹ Loss or compromise of distal circulation, necrosis of overlying skin, uncontrolled bleeding despite compression, and reversal of anticoagulation mandates emergent surgical intervention to repair the femoral pseudoaneurysm.

Arteriovenous fistulae

Femoral AVFs tend to persist in patients who are on steroids or suffer from chronic renal insufficiency. Implantation of covered stents in the femoral artery has been reported but appears to be contraindicated. As previously mentioned, there is considerable concern regarding complications of this approach, risks for restenosis, stent fracture due to frequent flexion in the groin region, and possible limitations for future femoral intervention.¹²³ Ongoing investigations will provide definitive understanding of the utility of this technique for managing femoral AVFs. In contrast to healthy concern about the durability of covered stent repairs in common femoral AVFs, the use of covered stents to manage iliac vein–iliac artery or aortocaval fistulas have been very effective.^124,125 Operative repair of a chronic AVF can be hazardous because of the friable nature of the vessels and the risk for considerable blood loss. Optimal treatment requires obliteration of the fistula and restoration of arterial and venous flow. At times, interposition grafting or patch angioplasty is needed to preserve flow without narrowing vessels. If there is a large defect in the vein, preoperative placement of arterial or venous balloons for intraoperative occlusion may help decrease hemorrhage during repair of the vessels feeding the fistula.