Christopher J. Dente and David V. Feliciano
The major sites of hemorrhage in patients sustaining blunt or penetrating abdominal trauma are the viscera, the mesentery, and the major abdominal vessels. The term abdominal vascular injury generally refers to injury to major intraperitoneal or retroperitoneal vessels and is generally classified into four zones described as follows and in Table 34-1:
TABLE 34-1 Classification of Abdominal Vascular Injury
• Zone 1: midline retroperitoneum
• Zone 2: upper lateral retroperitoneum
• Zone 3: pelvic retroperitoneum
• Porta hepatis/retrohepatic inferior vena cava
As many of these vessels are somewhat difficult to quickly access via a midline laparotomy incision, a systematic operative approach is required to adequately diagnose and manage these potentially devastating injuries. A general discussion of epidemiology and methods of diagnosis, with subsequent descriptions of the operative management of abdominal vascular injuries within each region of the abdomen, follows.
In reviews of vascular injuries sustained in military conflicts, abdominal vascular injuries have been extraordinarily rare. For example, DeBakey and Simeone’s classic article on 2,471 arterial injuries during World War II included only 49 that occurred in the abdomen, an incidence of 2%.1 Reporting on 304 arterial injuries from the Korean conflict, Hughes noted that only 7, or 2.3%, occurred in the iliac arteries.2In the review by Rich et al. of 1,000 arterial injuries in the Vietnam War, only 29, or 2.9%, involved abdominal vessels.3 Finally, a recent review of abdominal injuries during the Iraqi conflict documented only 4 injuries to major vessels in 145 patients undergoing laparotomy (2.8%).4
The data from civilian trauma centers are quite different. In 1979, 15% of patients with abdominal trauma treated at the Ben Taub General Hospital in Houston had injuries to major vascular structures.5 Also, abdominal vascular injury accounted for 27.5% of all arterial injuries treated over that same time period. A similar review from the same hospital in 1982 revealed that 31.9% of all vascular injuries occurred in the abdomen, including 18.5% of all arterial injuries and 47.5% of all venous injuries.6 Finally, a 30-year review (1958–1988) at the same hospital, published in 1989, documented that 33.8% of 5,760 cardiovascular injuries occurred in the abdomen.7 In the last 5 years of the period covered by the report (1984–1988), abdominal vascular injuries accounted for 27.3% of all cardiovascular injuries.
Even with the recent decrease in the volume of penetrating trauma in some centers, many patients with abdominal vascular injuries continue to be treated. For example, there were 302 patients with 238 abdominal arterial and 266 abdominal venous injuries who underwent operative repair at the Los Angeles County Hospital (University of Southern California) from 1992 to 1997.8 Similarly, there were 300 patients with 205 abdominal arterial and 284 abdominal venous injuries who underwent operative repair at the Grady Memorial Hospital (Emory University) from 1989 to 1998.9
The significantly higher number of abdominal vascular injuries treated in civilian as opposed to military practice likely reflects the modest wounding capacity of many handguns when compared with military ordinance, as well as the shorter prehospital transit times in most urban areas of the United States. Advances in military armor and the changing tactics of modern warfare also have led to a shift in injuries to the extremities rather than the torso, although noncompressible (torso) hemorrhage remained the leading cause of combatant death from hemorrhage in a recent review.10
At present, the estimated incidence of injury to major abdominal vessels in patients sustaining blunt abdominal trauma is thought to be about 5–10%.11,12 This is compared with patients with penetrating stab wounds to the abdomen, who will sustain a major abdominal vascular injury approximately 10% of the time (V. Spjut-Patrinely, D. V. Feliciano, Data from Ben Taub General Hospital, Houston, Texas, July 1985 to June 1988, unpublished), and patients with gunshot wounds to the abdomen, who will have injury to a major vessel 20–25% of the time.13
Rapid deceleration in motor vehicle crashes may cause two different types of vascular injuries in the abdomen. The first is avulsion of small branches from major vessels, with subsequent hemorrhage. A common example of this is the avulsion of intestinal branches from either the proximal or distal superior mesenteric artery at sites of fixation. A second type of vascular problem seen with deceleration injury is an intimal tear with secondary thrombosis of the lumen, such as is seen in patients with renal artery thrombosis, or a full-thickness tear with a secondary pseudoaneurysm of the renal artery.14–16
Crush injuries to the abdomen, such as by a lap seat belt or by a posterior blow to the spine, also may cause two different types of vascular injury. The first is an intimal tear or flap with secondary thrombosisof a vessel such as the superior mesenteric artery,17 infrarenal abdominal aorta,18,19 or iliac artery.20,21 The “seat belt aorta” is a classic example of an injury resulting from this mechanism.18,22 Direct blows can also completely disrupt exposed vessels, such as the left renal vein over the aorta23 or the superior mesenteric artery or vein at the base of the mesentery,24 leading to massive intraperitoneal hemorrhage, or even partly disrupt the infrarenal abdominal aorta, leading to a false aneurysm.25,26
Penetrating injuries, in contrast, create the same kinds of abdominal vascular injuries as are seen in the vessels of the extremities, producing blast effects with intimal flaps and secondary thrombosis, lateral wall defects with hemorrhage or pulsatile hematomas (early false aneurysms), or complete transection with either free bleeding or thrombosis.27 On rare occasions, a penetrating injury may produce an arteriovenous fistula involving the portal vein and hepatic artery, renal vessels, or iliac vessels.
Iatrogenic injuries to major abdominal vessels are an uncommon but persistent problem. Reported iatrogenic causes of abdominal vascular injury have included diagnostic procedures (angiography, cardiac catheterization, laparoscopy), abdominal operations (pelvic and retroperitoneal procedures), spinal operations (removal of a herniated disk), and adjuncts to cardiac surgery (cardiopulmonary bypass, intra-aortic balloon assist).28–30
History and Physical Examination
An abdominal vascular injury may present in one of three ways including free intraperitoneal hemorrhage, a contained intraperitoneal or retroperitoneal hematoma, and thrombosis of the vessel. As such, patients can be quickly divided into two major groups including those with ongoing hemorrhage and those without ongoing hemorrhage (contained hematoma or thrombosis). The presenting symptoms, thus, are variable based on both the event and the involved vessel. After blunt trauma, for example, free intraperitoneal hemorrhage may be seen with avulsion of mesenteric vessels and lead to secondary hypovolemic shock. Conversely, when thrombosis of the renal artery is present, the patient will be hemodynamically stable but may complain of upper abdominal and flank pain and will commonly have hematuria (70–80%).16 Thrombosis of the proximal superior mesenteric artery will cause severe abdominal pain, while thrombosis of the infrarenal abdominal aorta will cause pulseless lower extremities.
Penetrating truncal wounds between the nipples and the upper thighs remain the most common cause of abdominal vascular injuries. The exact vessel injured is generally related to the track of the missile or stab wound. For example, gunshot wounds directly on the midline most commonly involve the inferior vena cava or abdominal aorta. Gunshot wounds traversing the pelvis will often injure branches of the iliac artery or vein, while gunshot wounds in the right upper quadrant may involve the renovascular structures, vascular structures within the porta hepatis, or the retrohepatic inferior vena cava.
On physical examination, the findings in patients with abdominal vascular injury will obviously depend on whether a contained hematoma or active hemorrhage is present. Patients with contained hematomas in the retroperitoneum, base of the mesentery, or hepatoduodenal ligament, particularly those with injuries to abdominal veins, may be hypotensive in transit but often respond rapidly to the infusion of fluids. They may remain remarkably stable, with modest or even no peritoneal signs on examination, until the hematoma is opened at the time of laparotomy. These patients are candidates for the imaging studies mentioned below. Conversely, patients with active hemorrhage generally have a rigid abdomen and unrelenting hypotension. These patients should obviously undergo immediate laparotomy without further evaluation. In a review by Ingram et al. of 70 consecutive patients undergoing laparotomy for an abdominal vascular injury, patients could generally be divided into two groups based on an admission systolic blood pressure greater than or less than 100 mm Hg.31 In the former group, the mean base deficit on admission was −7.2, blood replacement in the operating room was 8.6 U, an isolated venous injury was present in 73.1% of patients, and survival was 96.2%. This was compared with a 43% survival and an average of 15.1 U of blood replacement in patients presenting with hypotension (Table 34-2). Indeed, admission base deficit was the only independent indicator of mortality in a recent series of patients with abdominal vascular injuries from Lincoln Hospital in New York City.32
TABLE 34-2 Blood Pressure in the Emergency Department in Patients with Abdominal Vascular Injury
The other major physical finding that may be noted in patients with abdominal vascular injury is loss of the pulse in the femoral artery in one lower extremity when the ipsilateral common or external iliac artery has been transected or is thrombosed. In such patients, the presence of a transpelvic gunshot wound associated with a wavering or an absent pulse in the femoral artery is pathognomonic of injury to the ipsilateral iliac artery.
In both stable and unstable patients, a rapid surgeon-performed ultrasound (Focused Assessment for the Sonographic Evaluation of the Trauma Patient [“FAST”]) is useful in ruling out an associated cardiac injury with secondary tamponade or an associated hemothorax mandating the insertion of a thoracostomy tube.33–36 In a stable patient with an abdominal gunshot wound, a routine flat-plate x-ray of the abdomen is of diagnostic value, so that the track of the missile can be predicted from markers placed over the wounds or from the position of a retained missile.
In former years, all patients who had suffered penetrating abdominal wounds and who were not in shock would undergo a one-shot intravenous pyelogram (IVP) in the emergency department. The major purposes of this study were as follows: to evaluate the function of both kidneys, with lack of flow to one kidney suggesting either absence of the kidney or thrombosis of the renal artery; the presence of active hemorrhage from the kidney itself; and the position and status of the ureters. This study is no longer performed routinely and is indicated only in stable patients with a flank wound and gross hematuria when the computed tomography (CT) scanner is not available.
In patients with blunt abdominal trauma, hematuria, modest to moderate hypotension, and peritonitis in the emergency department, a preoperative one-shot IVP during resuscitation would still be useful for documenting the presence of an intact kidney. If the kidney is mostly intact without extravasation of the dye, the surgeon will not have to open a perirenal hematoma at the subsequent laparotomy. Nonvisualization of one kidney on the IVP, suggesting thrombosis of the renal artery, was evaluated by renal arteriography in stable patients in the past. Experience with CT scanning of the abdomen in multiple patients with blunt trauma has documented that the absence of renal enhancement and excretion and the presence of a cortical rim sign are diagnostic of thrombosis of the renal artery, and arteriography is no longer indicated for this diagnosis.37 Similarly, any stable patient with blunt trauma who does not require an immediate laparotomy and who has significant hematuria should undergo an immediate abdominal CT scan without a preliminary one-shot IVP.38
Preoperative abdominal aortography should not be routinely performed to document intra-abdominal vascular injuries after penetrating wounds. This is because most patients with such wounds are not stable enough to undergo the manipulation required for appropriate studies of large vessels in an angiographic suite. In patients with blunt trauma, aortography is used to diagnose and treat deep pelvic arterial bleeding associated with fractures39 and to diagnose unusual injuries such as the previously mentioned intimal tears with thrombosis in the infrarenal aorta, the iliac artery, or the renal artery. The occasional patient is also a candidate for endovascular therapy and this will be discussed below.
As the technology of CT scanning has advanced, many surgeons and radiologists are comfortable making therapeutic decisions based on data acquired from multiplanar scanning and formal CT angiography. Extensive literature exists on the diagnosis of traumatic thoracic aortic disruption with CT40 and at least one small prospective study has shown acceptable accuracy of CT angiography in extremity trauma.41Conversely, data on the use of CT angiography as a method of diagnosis of abdominal vascular injury remain preliminary. Indeed, in one recent study, contrast-enhanced CT alone had a 94% sensitivity and 89% specificity for the diagnosis of active hemorrhage when compared with angiography.42 Most of the positive scans involved branches of the internal iliac artery with a concomitant pelvic fracture or injuries to solid organs and, thus, were not necessarily diagnostic of true abdominal vascular injury. Still, in the stable patient with blunt trauma, findings on CT that are suggestive of injury to the retroperitoneal great vessels warrant further evaluation with angiography or operative intervention.
INITIAL MANAGEMENT AND RESUSCITATION
Resuscitation in the field in patients with possible blunt or penetrating abdominal vascular injuries should be restricted to basic airway maneuvers such as intubation or cricothyroidotomy and decompression of a tension pneumothorax at the scene. Insertion of intravenous lines for infusing crystalloid solutions is best attempted during transport to the hospital. Restoration of blood pressure to normal levels is critical to neurologic recovery in the rare patients with associated blunt intracranial injuries and possible abdominal vascular injuries.43 In contrast, there is no consistent evidence to support either the aggressive administration of crystalloid solutions during the short prehospital times in urban environments or the withholding of similar solutions (“delayed resuscitation”) in patients with penetrating abdominal vascular injuries.44,45 Indeed, a key component of “damage control resuscitation” as espoused by the US military and discussed below is minimization of early crystalloid resuscitation.46
Emergency Department Resuscitation
In the emergency department, the extent of resuscitation clearly depends on the patient’s condition at the time of arrival. In the agonal patient with a rigid abdomen after a gunshot wound, emergency department thoracotomy with cross-clamping of the descending thoracic aorta may be necessary to maintain cerebral and coronary arterial flow, especially if the trauma operating room is geographically distant from the emergency department.47 Although all trauma surgeons agree that performing a thoracotomy in the emergency department will complicate the patient’s intraoperative course, the thoracotomy and cross-clamping are sometimes the only way to prevent irreversible ischemic changes in the patient’s brain and heart until a laparotomy with vascular control can be performed. It must be recognized, however, that the need for emergency department thoracotomy is essentially predictive of a <5% survival for the patient with blunt or penetrating abdominal trauma.48 In the large series by Feliciano et al.,47only 1 of 59 patients with isolated penetrating wounds to the abdomen survived after undergoing a preliminary thoracotomy in the emergency department.
In the patient arriving with blunt abdominal trauma, hypotension, and a positive surgeon-performed “FAST” or penetrating abdominal trauma and hypotension or peritonitis, a time limit of less than 5 minutes in the emergency department is mandatory. An identification bracelet is applied, an airway and thoracostomy tube are inserted if necessary, especially if the operating room is geographically distant, and blood samples for typing and cross-matching are obtained with the insertion of the first intravenous catheter. Whether more intravenous lines should be inserted in the emergency department or after arrival in the operating room is much debated. The authors have always believed that patients needing an emergency laparotomy should be in the operating room, as soon as the identification bracelet has been applied and a blood specimen has been sent to the blood bank.
There are now multiple large-bore catheters, specialized administration sets, and heating elements commercially available for use in the emergency department or operating room. With short, large-bore (10-gauge or number 8.5 French) catheters in peripheral veins, flow rates of 1,400–1,600 mL/min of crystalloid solutions can be obtained when an external pressure device is exerting 300 mm Hg pressure.49Blood replacement during resuscitation is usually with type-specific blood, although universal donor type O negative blood may be used when there is no time for even a limited cross-match.
Measures in the emergency department that will diminish the hypothermia of resuscitation include the following: a heated resuscitation room, the use of prewarmed (37–40°C [98.6–104.0°F]) crystalloid solutions, passage of all crystalloids and blood through high-flow warmers, and covering the patient’s trunk and extremities with prewarmed blankets or heating units.48–50
Damage Control Resuscitation and Massive Transfusion
In the last 5 years, based mostly on the military experience in Iraq, there has been a dramatic change in the resuscitation philosophy of critically injured patients in many centers. The military resuscitation philosophy of “damage control resuscitation” is seen as an extension of the concepts of “damage control surgery,” a term coined in the early 1990s by Rotondo et al.51 One cornerstone of damage control resuscitation is the early and aggressive use of either fresh whole blood or blood components (fresh frozen plasma and platelets) in high, defined ratios to packed red blood cells. In the civilian setting, this practice requires the support of the blood bank and a highly organized massive transfusion protocol (MTP). Multiple civilian centers have now published their results using institution-specific MTPs, generally with significant improvements in patient outcome.52–55 As many patients with abdominal vascular injury will require massive transfusion, the treating surgeons should be familiar with the design and implementation of any MTP that exists in their institution. The concepts of damage control surgery, damage control resuscitation, and massive transfusion will be covered in much more detail elsewhere in this text.
Draping and Incisions
In the operating room, the entire trunk from the chin to the knees is prepared and draped in the usual manner. Before making the incision for laparotomy, the trauma surgeon should confirm that the following items are available: blood components for transfusion, autotransfusion apparatus, a thoracotomy tray, an aortic compressor, a complete tray of vascular instruments, sponge sticks with gauze sponges in place for venous compression, as well as appropriate vascular sutures.
Maneuvers to Prevent or Decrease Hypothermia
In addition to the maneuvers previously described for preventing hypothermia in the emergency department, operative maneuvers with the same purpose include warming the operating room to >85°F (29.4°C); covering the patient’s head; covering the upper and lower extremities with a heating unit (Bair Hugger, Augustine Medical, Inc, Eden Prairie, Minnesota); the irrigation of nasogastric tubes, thoracostomy tubes, and open body cavities with warm saline; and the use of a heating cascade on the anesthesia machine.56
A preliminary operating room thoracotomy with cross-clamping of the descending thoracic aorta is used in some centers when the patient’s blood pressure on arrival is less than 70 mm Hg.57–59 As previously mentioned, this maneuver will maintain cerebral and coronary arterial flow if the heart is still beating and may prevent sudden cardiac arrest when abdominal tamponade is released. Unfortunately, it has little effect on intra-abdominal vascular injuries because of persistent bleeding from backflow. Indeed, patients with unrelenting shock after cross-clamping of the descending thoracic aorta essentially never survive.59
A midline abdominal incision is made, and all clots and free blood are manually evacuated or removed with suction. A rapid inspection is performed to visualize contained hematomas or areas of hemorrhage. One intra-abdominal physical finding that may be of diagnostic benefit to the surgeon is “black bowel,” which has been seen in patients with total transection or thrombosis of the proximal superior mesenteric artery. In a patient with a penetrating upper abdominal wound, a large hematoma in the supramesocolic area, and black bowel, an injury to the superior mesenteric artery is likely to be present.60
Active hemorrhage from solid organs is controlled by packing, while standard techniques of vascular control are used to control the active hemorrhage from major intra-abdominal vessels. Finger pressure, compression with laparotomy pads, grabbing the perforated artery with a hand (common or external iliac artery), or formal proximal and distal control is needed to control any actively hemorrhaging major artery. Similarly, options for control of bleeding from major veins such as the inferior vena cava, superior mesenteric vein, renal veins, or iliac veins include finger pressure, compression with laparotomy pads or sponge sticks, grabbing the perforated vein with a hand, applying Judd-Allis clamps to the edges of the perforation,61 and the application of vascular clamps. Once hemorrhage from the vascular injuries is controlled in patients with penetrating wounds, it may be worthwhile to rapidly apply Babcock clamps, Allis clamps, or noncrushing intestinal clamps, or to rapidly use a surgical stapler to control as many gastrointestinal perforations as possible to avoid further contamination of the abdomen during the period of vascular repair. The abdomen is irrigated with an antibiotic–saline solution, the vascular repair is then performed, a soft tissue cover is applied over the repair, and the remainder of the operation is directed toward repair of injuries to the bowel and solid organs.
Conversely, if the patient has a contained retroperitoneal hematoma at the time of laparotomy, the surgeon occasionally has time to first perform necessary gastrointestinal repairs in the free peritoneal cavity, change gloves, and irrigate with an antibiotic–saline solution. The surgeon can then open the retroperitoneum to expose the underlying abdominal vascular injury.
Hematomas or hemorrhage associated with abdominal vascular injuries generally occur in zone 1, midline retroperitoneum; zone 2, upper lateral retroperitoneum; zone 3, pelvic retroperitoneum; or the portal–retrohepatic area of the right upper quadrant, as previously described (Table 34-1). The magnitude of injury is best described using the Organ Injury Scale of the American Association for the Surgery of Trauma (AAST).62
MANAGEMENT OF INJURIES IN ZONE 1: SUPRAMESOCOLIC REGION
Exposure and Vascular Control
The midline retroperitoneum of zone 1 is divided by the transverse mesocolon into a supramesocolic region and an inframesocolic region. If a hematoma or hemorrhage is present in the midline supramesocolic area, injury to the suprarenal aorta, celiac axis, proximal superior mesenteric artery, or proximal renal artery should be suspected. In such cases, there are several techniques for obtaining proximal vascular control of the aorta at the hiatus of the diaphragm. When a contained hematoma is present, as it frequently is with wounds to the aorta in the aortic hiatus, the surgeon usually has time to reflect all left-sided intra-abdominal viscera, including the colon, kidney, spleen, tail of the pancreas, and fundus of the stomach to the midline (left-sided medial visceral rotation) (Fig. 34-1).63–66 The advantage of this technique is that it provides extensive exposure for visualization of the entire abdominal aorta from the aortic hiatus of the diaphragm to the aortic bifurcation. Disadvantages include the time required to complete the maneuver (5–7 minutes), risk of damage to the spleen, left kidney, or posterior left renal artery during the maneuver, and a fold in the aorta that results when the left kidney is rotated anteriorly. One alternative is to leave the left kidney in its fossa, thereby eliminating potential damage to or distortion resulting from rotation of this structure. In either case, this maneuver provided the best exposure and allowed for the greatest survival in a series of 46 patients with suprarenal aortic injuries studied at Ben Taub General Hospital in Houston, Texas, in the 1970s.65
FIGURE 34-1 Left medial visceral mobilization is performed in the retroperitoneal plane behind all left-sided intra-abdominal viscera in a patient with a supramesocolic hematoma in the midline. (Reproduced with permission from Feliciano DV. Truncal vascular trauma. In: Callow AD, Ernst CB, eds. Vascular Surgery. Theory and Practice. Stamford, CT: Appleton & Lange; 1995:1059–1085. © The McGraw-Hill Companies, Inc.)
Because of the dense nature of the celiac plexus of nerves connecting the right and left celiac ganglia as well as the lymphatics that surround the supraceliac aorta, it is frequently helpful to transect the left crus of the aortic hiatus of the diaphragm at the 2 o’clock position to allow for exposure of the distal descending thoracic aorta above the hiatus.67 With the distal descending thoracic aorta in the hiatus exposed, a supraceliac aortic clamp can be applied without difficulty. This allows for the extra few centimeters of exposure that is essential for complex repair of the vessels within this tightly confined anatomic area.
Conversely, if active hemorrhage is coming from this area, the surgeon may attempt to control it manually or with one of the aortic compression devices.68,69 Failing this, an alternate approach is to divide the lesser omentum manually, retract the stomach and esophagus to the left, and digitally separate the muscle fibers of the aortic hiatus of the diaphragm from the supraceliac aorta to obtain similar, if not more, limited exposure as described for the left-sided medial visceral rotation, but more quickly.70 After either approach to the suprarenal abdominal aorta, cross-clamp time should be minimized to avoid the primary fibrinolytic state that occurs, presumably due to hepatic hypoperfusion.71 Distal control of the aorta in this location is awkward because of the presence of the celiac axis and superior mesenteric artery (Fig. 34-2). In some patients with injury confined to the supraceliac aorta, the celiac axis may have to be divided and ligated to allow for more space for the distal aortic clamp and subsequent vascular repair. Necrosis of the gallbladder is a likely sequela, and cholecystectomy is generally warranted, although this may be done at repeat exploration when “damage control” techniques are required.72
FIGURE 34-2 (A) View of suprarenal aorta and major branches after left-sided medial mobilization maneuver. (B) Diagrammatic representation of structures with labels. (Reproduced with permission from Baylor College of Medicine.)
With small perforating wounds to the aorta at this level, lateral aortorrhaphy with 3-0 or 4-0 polypropylene suture is preferred. If two small perforations are adjacent to one another, they should be connected and the defect closed in a transverse fashion with the polypropylene suture. When closure of the perforations results in significant narrowing, or if a portion of the aortic wall is missing, patch aortoplasty with polytetrafluoroethylene (PTFE) is indicated. The other option is to resect a short segment of the injured aorta and attempt to perform an end-to-end anastomosis. Unfortunately, this is often impossible because of the limited mobility of both ends of the aorta at this level.
On rare occasions, patients with extensive injuries to the diaphragmatic or supraceliac aorta will require insertion of a synthetic vascular conduit or spiral graft after resection of the area of injury.73–75 Many of these patients have associated gastric, enteric, or colonic injuries, and much concern has been expressed about placing a synthetic conduit, such as a 12-, 14-, or 16-mm woven Dacron, albumin-coated Dacron, or PTFE prosthesis, in the abdominal aorta (Fig. 34-3). The data in the American literature describing young patients with injuries to nondiseased abdominal aortas do not support the concern about Dacron interposition grafts, and there are few reports describing the use of PTFE grafts in penetrating trauma to the abdominal aorta. Despite the available data, some clinicians continue to recommend an extra-anatomic bypass when injury to the abdominal aorta would require replacement with a conduit in the presence of gastrointestinal contamination.22
FIGURE 34-3 A 22-year-old man with a gunshot wound to the right upper quadrant had injuries to the prepyloric area of the stomach and to the supraceliac abdominal aorta. The aortic injury was managed by segmental resection and replacement with a 16-mm polytetrafluoroethylene (PTFE) graft. The patient was discharged 46 days after injury. (Reproduced with permission from Feliciano DV. Injuries to the great vessels of the abdomen. In: Holcroft JW, ed. Scientific American Surgery. Trauma Section. New York: Scientific American; 1998:1–12.)
As previously noted, repairs of the intestine and the aorta should not be performed simultaneously. Once the perforated bowel has been packed away and the surgeon has changed gloves, the aortic prosthesis is sewn in place with 3-0 or 4-0 polypropylene suture. After appropriate flushing of both ends of the aorta and removal of the distal aortic clamp, the proximal aortic clamp should be removed very slowly as the anesthesiologist rapidly infuses fluids. If a long aortic clamp time has been necessary, the prophylactic administration of intravenous bicarbonate is indicated to reverse the “washout” acidosis from the previously ischemic lower extremities.76 The retroperitoneum is then copiously irrigated and closed in a watertight fashion with an absorbable suture.
Cross-clamping of the supraceliac aorta in a patient with hemorrhagic shock results in severe ischemia of the lower extremities. Restoration of arterial inflow will then cause a reperfusion injury. In a patient who is hemodynamically stable after repair of the suprarenal (or infrarenal) abdominal aorta, measurement of compartmental pressures below the knees should be performed before the patient is moved from the operating room. Pressures in the range of 30–35 mm Hg should be treated with below-knee, two-incision, four-compartment fasciotomies.77
The survival rate of patients with penetrating injuries to the suprarenal abdominal aorta in eight series published from 1974 to 1992 was 34.8%65,75,78–83 (Table 34-3). Four more recent reviews have documented a significant decline in survival for injuries to the abdominal aorta (suprarenal and infrarenal), ranging from 21.1% to 50% (mean 30.2%) even when patients with exsanguination before repair or those treated with ligation only were excluded.8,9,84,85 In one series in which injuries to the suprarenal and infrarenal abdominal aorta were separated, the survival rate in the suprarenal group was only 8.3% (3/36).84 The reasons for this decrease in survival figures are not defined in the reviews described, although a likely cause is the shorter prehospital times for exsanguinated patients that have been realized with improvements in emergency medical services.
TABLE 34-3 Survival with Injuries to the Abdominal Aorta
Blunt injury to the suprarenal aorta is extraordinarily rare. While blunt injury to the descending thoracic aorta is well described throughout the trauma literature, only 62 cases of blunt trauma to the abdominal aorta were found by Roth et al. in a literature review in 1997.22 Of these, only one case was noted to be in the suprarenal aorta. The most common location is between the origin of the inferior mesenteric artery and the aortic bifurcation (see below). These injuries generally present with signs and symptoms of aortic thrombosis, rather than hemorrhage, with the most common signs being a lack of femoral pulses (81%), abdominal tenderness (55%), lower extremity weakness or paralysis (47%), and paresthesias (20%).22 Management of these injuries is discussed more extensively in Section “Infrarenal Aorta.”
Injury to the celiac axis is rare. One of the largest series in the literature, reported by Asensio et al., documented the treatment of 13 patients with this uncommon injury.86 Penetrating injuries were the cause in 12 patients, and overall mortality was 62%. Eleven patients were treated with ligation and one with primary repair, with the final patient exsanguinating prior to therapy. Of the five survivors, four had undergone ligation, and all deaths occurred in the operating room. This group also performed an extensive literature review and could only document 33 previously reported cases, all the result of penetrating trauma. Furthermore, they could find no survivor treated with any sort of complex repair.86 One case of injury to the celiac artery after blunt trauma was reported by Schreiber et al. and occurred in a patient with preexisting median arcuate ligament syndrome.87 Given these results, patients with injuries to the celiac axis that are not amenable to simple arteriorrhaphy should undergo ligation, which should not cause any short-term morbidity other than the aforementioned risk of gallbladder necrosis.
When branches of the celiac axis are injured, they are often difficult to repair because of the dense neural and lymphatic tissue in this area and the small size of the vessels in a patient in shock with secondary vasoconstriction. There is clearly no good reason to fix major injuries to either the left gastric or proximal splenic artery in the patient with trauma to this area. In both instances, these vessels should be ligated. The common hepatic artery may have a larger diameter than the other two vessels, and an injury to this vessel may occasionally be amenable to lateral arteriorrhaphy, end-to-end anastomosis, or the insertion of a saphenous vein or prosthetic graft. In general, however, one should not worry about ligating the hepatic artery proper proximal to the origin of the gastroduodenal artery, since the extensive collateral flow from the midgut through this vessel will maintain the viability of the liver.
Superior Mesenteric Artery
Injuries to the superior mesenteric artery are managed based on the level of injury. In 1972, Fullen et al.88 described an anatomic classification of injuries to the superior mesenteric artery that has been used intermittently by subsequent authors in the trauma literature.60,89 If the injury to the superior mesenteric artery is beneath the pancreas (Fullen zone 1), the pancreas may have to be transected between Glassman and Dennis intestinal clamps to control the bleeding point. Because the superior mesenteric artery has few branches at this level, proximal and distal vascular control is relatively easy to obtain once the overlying pancreas has been divided. Another option is to perform medial rotation of the left-sided intra-abdominal viscera, as previously described, and apply a clamp directly to the proximal superior mesenteric artery at its origin from the left side of the aorta. In this instance, the left kidney may be left in the retroperitoneum as the medial rotation is performed.
Injuries to the superior mesenteric artery also occur beyond the pancreas at the base of the transverse mesocolon (Fullen zone 2, between the pancreaticoduodenal and middle colic branches of the artery). Although there is certainly more space in which to work in this area, the proximity of the pancreas and the potential for pancreatic leaks near the arterial repair make injuries in this location almost as difficult to handle as the more proximal injuries.60,88,89 If the superior mesenteric artery has to be ligated at its origin from the aorta or beyond the pancreas (Fullen zone 1 or 2), collateral flow from both the foregut and hindgut should maintain theoretically the viability of the midgut in the distribution of this vessel.90 In truth, however, exsanguinating hemorrhage from injuries in this area often leads to intense vasoconstriction of the more distal superior mesenteric artery. For this reason, collateral flow is often inadequate to maintain viability of the distal midgut, especially the cecum and ascending colon. In the hemodynamically unstable patient with hypothermia, acidosis, and a coagulopathy, the insertion of a temporary intraluminal shunt into the debrided ends of the superior mesenteric artery is most appropriate and fits the definition of damage control.91 If replacement of the proximal superior mesenteric artery is necessary in a more stable patient, it is safest to place the origin of the saphenous vein or prosthetic graft on the distal infrarenal aorta, away from the pancreas and other upper abdominal injuries (Fig. 34-4).60 A graft in this location should be tailored so that it will pass through the posterior aspect of the mesentery of the small bowel and then be sutured to the superior mesenteric artery in an end-to-side fashion without significant tension. It is mandatory to cover the aortic suture line with retroperitoneal fat or a viable omental pedicle to avoid an aortoduodenal or aortoenteric fistula at a later time. This is much easier to perform if the proximal origin of the graft is located on the distal aorta. Injuries to the more distal superior mesenteric artery (Fullen zone 3, beyond the middle colic branch, and zone 4, at the level of the enteric branches) should be repaired, since ligation in this area is distal to the connection to collateral vessels from the foregut and the hindgut.92This may require microsurgical techniques.93 If this cannot be accomplished because of the small size of the vessel, ligation may mandate extensive resection of the ileum and right colon.
FIGURE 34-4 (A) When complex grafting procedures to the superior mesenteric artery are necessary, it may be dangerous to place the proximal suture line near an associated pancreatic injury. (B) The proximal suture line should be on the lower aorta, away from the upper abdominal injuries, and should be covered with retroperitoneal tissue. (Reproduced from Accola KD, Feliciano DV, Mattox KL, et al. Management of injuries to the superior mesenteric artery. J Trauma. 1986;26:313.)
The survival rate of patients with penetrating injuries to the superior mesenteric artery in six series published from 1972 to 1986 was 57.7% (Table 34-4).60,81,86,94–96 Four more recent reviews, including a large multi-institutional study,89 had a mean survival of 58.7%.8,9,84,89 In one of the older series, survival decreased to 22% when any form of repair more complex than lateral arteriorrhaphy was performed.60Independent risk factors for mortality in the multi-institutional study included injury to Fullen zone 1 or 2, transfusion of >10 U of packed red blood cells, intraoperative acidosis or dysrhythmias, and multisystem organ failure.89
TABLE 34-4 Survival with Injuries to the Superior Mesentery Artery
Proximal Renal Arteries
Injuries to the proximal renal arteries may also present with a zone 1, supramesocolic hematoma or with hemorrhage in this area. The left medial visceral rotation maneuver described earlier allows visualization of much of the posterior left renal artery from the aorta to the kidney. This maneuver does not, however, allow for visualization of the proximal right renal artery. The proximal vessel is best approached through the base of the mesocolon beneath the left renal vein and between the infrarenal abdominal aorta and inferior vena cava. Options for repair of either the proximal or distal renal arteries are described later in this chapter (Section “Management of Injuries in Zone 2”).
Superior Mesenteric Vein
One other major abdominal vessel, the proximal superior mesenteric vein, lying to the right of the superior mesenteric artery, may be injured at the base of the mesocolon. Injury to the most proximal aspect of this vessel near its junction with the splenic vein is difficult to manage. The overlying pancreas, proximity of the uncinate process, and close association with the superior mesenteric artery often preclude easy access to proximal and distal control of the vein. Therefore, as with injuries to the proximal superior mesenteric artery, the neck of the pancreas may have to be transected between noncrushing vascular and intestinal clamps to gain access to a perforation. More commonly, the surgeon will find a perforation inferior to the lower border of the pancreas. Often, the vein can be compressed manually or squeezed between the surgeon’s fingers as an assistant places a continuous row of 5-0 polypropylene sutures into the edges of the perforation. If a posterior perforation is present, multiple collaterals entering the vein at this point will have to be ligated to roll the perforation into view. Occasionally, the vein will be nearly transected and both ends will have to be controlled with vascular clamps. With an assistant pushing the small bowel and its mesentery back toward the pancreas, the surgeon can reapproximate the ends of the vein without tension.
When multiple vascular and visceral injuries are present in the upper abdomen and the superior mesenteric vein has been severely injured, ligation can be performed in the young trauma patient. In three older reviews of injuries to the portal venous system, ligation of the superior mesenteric vein was performed in 27 patients, and 22 survived.81,97,98 In one review of injuries to the superior mesenteric vein, survival was 85% among 33 patients treated with ligation versus 64% in 77 patients who underwent repair.99 Stone et al. have emphasized the need for vigorous postoperative fluid resuscitation in these patients as splanchnic hypervolemia leads to peripheral hypovolemia for at least 3 days after ligation of the superior mesenteric vein.98 The survival rate of patients with injuries to the superior mesenteric vein in four series published from 1978 to 1983 was 72.1% (Table 34-5).81,96–98 Three more recent reviews had a mean survival of 58.3%.8,9,84
TABLE 34-5 Survival with Injuries to the Superior Mesenteric Vein
MANAGEMENT OF INJURIES IN ZONE 1: INFRAMESOCOLIC REGION
Exposure and Vascular Control
The second major area of hematoma or hemorrhage in the midline is the inframesocolic area. In this location, abdominal vascular injuries include those to the infrarenal abdominal aorta or inferior vena cava. Exposure of an inframesocolic injury to the aorta is obtained by duplicating the maneuvers used to gain proximal aortic control during the elective resection of an abdominal aortic aneurysm. The transverse mesocolon is pulled up toward the patient’s head, the small bowel is eviscerated toward the right (surgeon’s) side of the table, and the midline retroperitoneum is opened until the left renal vein is exposed. A proximal aortic clamp should then be placed immediately inferior to the left renal vein. When a large retroperitoneal hematoma is present and proximal inframesocolic control is difficult to obtain, it should always be remembered that the hole in the aorta is under the highest point of the hematoma (“Mount Everest phenomenon”). Therefore, rapid finger splitting of the hematoma will generally bring the surgeon directly to the area of injury. Exposure to allow for application of the distal vascular clamp is obtained by dividing the midline retroperitoneum down to the aortic bifurcation, carefully avoiding the left-sided origin of the inferior mesenteric artery. This vessel, however, may be sacrificed whenever necessary for exposure.
If the aorta is intact and an inframesocolic hematoma appears to be more extensive on the right side of the abdomen than on the left, or if there is active hemorrhage coming through the base of the mesentery of the ascending colon or hepatic flexure of the colon, injury to the inferior vena cava caudad to the liver should be suspected. Although it is possible to visualize the vena cava through the midline retroperitoneal incision previously described, most trauma surgeons are more comfortable in visualizing the vena cava by mobilizing the right half of the colon and C-loop of the duodenum and leaving the right kidney in situ (right medial visceral rotation) (Fig. 34-5). This permits the entire vena caval system from the confluence of the iliac veins to the suprarenal vena cava below the liver to be visualized. It is often difficult to define precisely where a hole is in a large vein of the abdomen, such as the inferior vena cava, until much of the loose retroperitoneal fatty tissue is stripped away from the wall of the vessel. Once this is done, the site of hemorrhage can be localized.
FIGURE 34-5 Medial mobilization of right-sided intra-abdominal viscera except the kidney allows for visualization of the entire infrahepatic inferior vena cava. (Reproduced with permission from Baylor College of Medicine.)
If active hemorrhage appears to be coming from the anterior surface of the vena cava, a Satinsky-type vascular clamp should be applied directly to the perforation as it is elevated by a pair of vascular forceps or Allis clamps. When the vena cava has been extensively lacerated and partial occlusion cannot be performed, it is often helpful to compress the proximal and distal vena cava around the partial transection or extensive laceration using gauze sponges placed in straight sponge sticks. Because of back-bleeding from lumbar veins, it may be necessary to use large DeBakey aortic clamps and completely occlude the vena cava above and below some injuries. This maneuver carries a risk in the already hypotensive patient, since venous return to the right side of the heart is significantly impaired. For this reason, one should consider simultaneous clamping of the infrarenal abdominal aorta.
The two areas in which proximal and distal control of the inferior vena cava below the liver is especially difficult to obtain are at the confluence of the common iliac veins and at the caval junction with the renal veins. Although sponge stick compression of the common iliac veins and the vena cava superiorly may control hemorrhage at the confluence, visualization of perforating wounds in this area is compromised by the overlying aortic bifurcation. In the case of difficult exposure, one technique is to divide and ligate the right internal iliac artery, which may allow for lateral and cephalad retraction of the right common iliac artery to expose the venous injury. An alternate and interesting approach, but one that is rarely necessary, is the temporary division of the overlying right common iliac artery itself, with mobilization of the aortic bifurcation to the left.100 This technique provides wide exposure of the confluence of the common iliac veins and the distal vena cava and the venous injury can then be repaired in the usual fashion. The right common iliac artery is reconstituted by an end-to-end anastomosis.
When the perforation occurs at the junction of the renal veins and the inferior vena cava, it should be directly compressed with either sponge sticks or the fingers. An assistant then clamps or compresses the infrarenal vena cava and the suprarenal infrahepatic vena cava and loops both renal veins individually with vascular tapes to allow for the direct application of angled vascular clamps. When time does not allow for this dissection, medial mobilization of the right kidney may allow for the application of a partial occlusion clamp across the inferior vena cava at its junction with the right renal vein. This medial mobilization maneuver is also useful for exposing posterior perforations in the suprarenal infrahepatic vena cava.101 Should this latter maneuver be performed, care must be taken to divide and ligate but not avulse the first lumbar vein on the right as it frequently enters the junction of the right renal vein and inferior vena cava. One other useful technique for controlling hemorrhage from the inferior vena cava in all locations is to use a Foley balloon catheter for tamponade.102–105 Either a 5-mL or a 30-mL balloon catheter can be inserted into a caval laceration, the balloon inflated in the lumen, and traction applied to the catheter. Once the bleeding is controlled, either a purse-string suture is inserted or a transverse venorrhaphy is performed, taking care not to rupture the underlying balloon with the needle. The balloon catheter is then deflated and removed just before completion of the suture line.
As with injuries to the suprarenal aorta, penetrating or blunt injuries in the infrarenal abdominal aorta are repaired primarily with 3-0 or 4-0 polypropylene sutures or by patch aortoplasty, end-to-end anastomosis, or insertion of a woven Dacron graft, albumin-coated Dacron graft, or a PTFE graft—none of which require preclotting. Because of the small size of the aorta in young trauma patients, it is unusual to be able to place a tube graft larger than 12, 14, or 16 mm in diameter if one is required, as previously noted. The principles of completing the suture lines and flushing are exactly the same as for aortic repairs in the suprarenal area. Since the retroperitoneal tissue is often thin in young patients, it may be worthwhile to cover an extensive aortic repair or the suture line of a prosthesis with mobilized omentum before closure of the retroperitoneum.106 After mobilization of the gastrocolic omentum off the transverse colon, it can be placed into the lesser sac superiorly and then brought down through a hole in the transverse mesocolon over the repair or graft in the infrarenal aorta. An alternate approach is to mobilize the gastrocolic omentum off the right side of the transverse colon and then bring the mobilized pedicle into the area just below the ligament of Treitz to once again cover the aortic repair or graft. This vascularized pedicle of omentum should prevent a postoperative aortoduodenal fistula.
While the vast majority of injuries to the infrarenal aorta are penetrating in nature, a small number occur after blunt trauma. In the aforementioned review of 62 cases of blunt aortic trauma prior to 1997 reported by Roth et al., motor vehicle collisions accounted for 57% of the cases and 47% of the total were directly attributed to lap belts.22 The patients generally present with symptoms of acute arterial insufficiency as stated above, although a small number present in a delayed fashion with claudication, impotence, or, rarely, delayed rupture.22,107,19
The survival rate of patients with injuries to the infrarenal abdominal aorta in six series published from 1974 to 1992 was 46.2% (Table 34-3).78,80–83,108 As previously noted in the discussion of recent decreases in survival figures for injuries to the suprarenal abdominal aorta, the same has been true for injuries to the infrarenal abdominal aorta. In the one series, published in 2001, in which injuries to the suprarenal and infrarenal abdominal aorta were separated, the survival rate in the infrarenal group was only 34.2%.84
One peculiar and fortunately rare injury to the infrarenal abdominal aorta is rupture of a preexisting aortic aneurysm or distal embolization from an aneurysm secondary to blunt abdominal trauma.109,110
Infrahepatic Inferior Vena Cava
Anterior perforations of the inferior vena cava are best repaired in a transverse fashion using a continuous suture of 4-0 or 5-0 polypropylene. If vascular control is satisfactory and a posterior perforation can be visualized adequately by extending the anterior perforation, the posterior perforation can be repaired from inside the vena cava, with the first suture knot outside the lumen. When a significant longitudinal perforation is present, especially when adjacent perforations have been joined, the repaired vena cava will often take on the appearance of an hourglass. This narrowing may lead to slow postoperative occlusion of the vena cava. In the unstable patient who has developed a coagulopathy, no further attempt should be made to modify the repair. In the stable patient, there may be some justification for applying a large venous patch taken from either the resected inferior mesenteric vein or an ovarian vein or applying a PTFE patch.
In the case of a young patient who is exsanguinating and in whom extensive repair of the infrarenal inferior vena cava appears to be necessary, ligation of this vessel is usually well tolerated as long as certain precautions are taken. The first of these is to measure the pressures in the anterior compartments of the legs and to perform bilateral below-knee four-compartment fasciotomies at the first operation if the pressure is 30–35 mm Hg, depending on the patient’s hemodynamic status. Bilateral thigh fasciotomies may be necessary, as well, within the first 48 hours after ligation. The second is to maintain circulating volume in the postoperative period through infusion of the appropriate fluids. The third is to apply elastic compression wraps to both lower extremities and keep them continuously elevated for approximately 5–7 days after operation. Patients should wear the wraps when they start to ambulate, as well. If there is some residual edema even with the wraps in place at the time of hospital discharge, the patient should be fitted with full-length, custom-made support hose. In a recent review of 100 injuries to the inferior vena cava, 25 underwent ligation, including 22 with injuries to the infrarenal vena cava. Survival to hospital discharge was 41%, and 1-year follow-up was available in seven of nine survivors and no patient had more than trace lower extremity edema.111 While the majority of patients, therefore, seem to have no or minimal long-term edema, there have been occasional reports of severe edema in the postoperative period that has required later interposition grafting.112
Ligation of the suprarenal inferior vena cava is performed only when the patient has an extensive injury at this location and appears to have terminal shock at operation. In the above-mentioned series, three patients underwent ligation of the suprarenal inferior vena cava with only one long-term survivor. This patient required dialysis over his hospital course but gradually had a return of his renal function and was discharged without renal insufficiency. One-year follow-up in this patient revealed minimal lower extremity edema and normal renal function.111 Similarly, one other report described a patient treated with suprarenal ligation who did not develop acute renal failure and who continued to do well 2 years after injury.106 In order to avoid the risk of acute renal failure and massive edema of the lower half of the body that would ordinarily be associated with ligation at this level, several innovative approaches have been used. These include suprarenal insertion of a saphenous vein composite interposition graft, insertion of a Dacron or PTFE interposition graft, or insertion of a cavo-right atrial Dacron or PTFE bypass graft.112–114 While long-term data are lacking for both Dacron and PTFE interposition or bypass grafts in the major veins of the abdomen, the use of an externally supported PTFE graft in combination with chronic anticoagulation would presumably offer the best long-term patency.
Survival rates for patients with injuries to the inferior vena cava obviously depend on the location of injury. Survival after retrohepatic injury is rare, with only one survivor in the most recent series.111 If one eliminates injuries to the supradiaphragmatic and retrohepatic vena cava from seven series published from 1978 to 1994, the average survival for 515 patients with injuries to the infrahepatic vena cava was 72.2%.81,83,101,115–118 Further eliminating juxtarenal injuries, the average survival for 318 patients with true infrarenal caval injuries was 76.1% (Table 34-6).81,83,101,115–118 The two more recent series, in which injuries are stratified by location, again show lower overall survival rates (40–60%, Table 34-6).84,111 Finally, short-term patency of repair of the inferior vena cava has been studied by Porter et al.119 In 28 patients with prior lateral venorrhaphy of the inferior vena cava, patency of the cava was documented by sonography, CT scan, or both in 24 (86%).
TABLE 34-6 Survival with Injuries to the Inferior Vena Cavaa
MANAGEMENT OF INJURIES IN ZONE 2
Exposure and Vascular Control
If a hematoma or hemorrhage is present in the upper lateral retroperitoneum, injury to the renal artery, renal vein, or both, as well as injury to the kidney, should be suspected. Most patients with penetrating trauma to the abdomen are explored prior to extensive radiologic work-up; however, in selected patients who are hemodynamically stable after sustaining penetrating wounds to the flank, CT scan has been used to document an isolated minor renal injury and operation has been avoided.120 Conversely, patients found to have a perirenal hematoma at the time of exploration for a penetrating abdominal wound should have unroofing of the hematoma and exploration of the wound track. If the hematoma is not rapidly expanding and there is no free intraabdominal bleeding, some surgeons will loop the ipsilateral renal artery with a vascular tape in the midline at the base of the mesocolon.121 The left renal vein can be looped with a vascular tape in the same location; however, vascular control of the proximal right renal vein will have to wait for mobilization of the C-loop of the duodenum and unroofing of the vena cava at its junction with the renal veins. It should be noted that obtaining proximal vascular control prior to exploration of a perirenal hematoma is controversial. Indeed, in one study, preliminary vascular control of the renal hilum had no impact on nephrectomy rate, transfusion requirements, or blood loss.122
Conversely, if there is active bleeding from the kidney through Gerota’s fascia or from the retroperitoneum overlying the renal vessels, central renovascular control is not obtained. The surgeon should simply open the retroperitoneum lateral to the injured kidney and manually elevate the kidney directly into the wound. A large vascular clamp can be applied proximal to the hilum either at the midline on the left or just lateral to the inferior vena cava on the right to control any further bleeding.
Patients who present after blunt trauma may also have either a renovascular or renal parenchymal injury. Patients in the former group, however, generally present with renovascular occlusion, which will be discussed below. In patients who have suffered blunt abdominal trauma and have undergone a preoperative IVP, renal arteriogram, or CT of the kidneys that has demonstrated flow to the kidney and/or a low Organ Injury Scale grade of injury, there is no justification for exploring the perirenal hematoma should an emergency laparotomy be indicated for other reasons.
Renovascular Injuries: Renal Artery
Renovascular injuries are difficult to manage, especially when the renal artery is involved. It is an extraordinarily small vessel that is deeply embedded in the retroperitoneum. Occasionally, small perforations of the artery from penetrating wounds can be repaired by lateral arteriorrhaphy or resection with an end-to-end anastomosis. Interposition grafting using either a saphenous vein or PTFE graft for extensive injuries is indicated only when there appears to be a reasonable hope for salvage of the kidney. Borrowed arteries, such as the splenic artery to replace the left renal artery and the hepatic artery to replace the right renal artery, have been used rarely, but are not often indicated in hypotensive trauma patients with significant renovascular injuries from penetrating wounds.123 In these patients and those with multiple intra-abdominal injuries or a long preoperative period of ischemia, nephrectomy may be a better choice, as long as intraoperative palpation has confirmed a normal contralateral kidney. The survival rate of patients with injuries to the renal arteries from penetrating trauma in two older studies was approximately 87%, with renal salvage in only 30–40%.121,124 In three more recent series, the survival rate was 65.1%.8,9,84
Diagnosis of patients with blunt injury to the renal artery is more difficult. Intimal tears in the renal arteries may result from deceleration in motor vehicle crashes, automobile–pedestrian accidents, and falls from heights. These usually lead to secondary thrombosis of the vessel and complaints of upper abdominal and flank pain as previously noted. One older literature review noted that only 30% of patients with intimal tears in the renal arteries had gross hematuria, 43% had microscopic hematuria, and 27% had no blood in the urine.125 Hence, the diagnosis may be missed, because a CT scan may not be performed expeditiously in stable patients with normal abdominal examinations.
If either an IVP or CT scan documents occlusion of a renal artery, the surgeon must decide on the need for either operation or endovascular intervention. The time interval from the episode of trauma appears to be the most critical factor in saving the affected kidney.121 In one study, there was an 80% chance of restoring some renal function at 12 hours, but this dropped to 57% at 18 hours after the onset of occlusion.125 In a recent series, only two of five kidneys were salvaged after attempted revascularization, with one early salvage requiring a late nephrectomy at 6 months for severe hypertension, leading to a long-term salvage rate of only one kidney (20%). Of interest, only three of seven patients not undergoing revascularization required late nephrectomy.16
If surgery is performed, extensive mobilization of the injured renal artery will usually allow a limited resection of the area of the intimal tear 2–3 cm from the abdominal aorta, with an end-to-end anastomosis for reconstruction. Alternate approaches are nephrectomy, perfusion of the kidney with Euro-Collins solution, and autotransplantation.118 The latter approach is obviously only applicable to stable patients who, ideally, have isolated injuries. Documentation of a successful result is usually not possible until acute tubular necrosis resolves over several weeks.126 Endovascular techniques designed to revascularize the kidneys after renal artery injury are discussed below.
It is of interest that case reports in the literature have documented either spontaneous recovery or the late successful revascularization of one or both kidneys after presumed blunt thrombosis of the renal artery.127 The authors of the report suggest that attempts at late revascularization may be occasionally rewarding and advise that early nephrectomy is unnecessary because of the low incidence of chronic hypertension in cases of renal artery thrombosis.127
In summary, because of the poor renal salvage rates after blunt occlusion of the renal artery discussed above, there is decreasing interest in operative renal revascularization especially after a delayed diagnosis or in a patient with a unilateral injury. Therefore, patients with injuries to only one renal artery should be considered for revascularization only if they are stable and have short warm ischemia times, ideally less than 5 hours. Other patients, assuming they have a normally functioning contralateral kidney, should be either observed or considered for endovascular procedures. Obviously, patients with bilateral renal artery injuries or those with injuries to a solitary kidney should be strongly considered for revascularization. In addition, prolonged follow-up should be arranged for all patients, as some of them will develop hypertension.16
Renovascular Injuries: Renal Vein
Although blunt avulsion injuries of the renal vein may result in exsanguination, patients with penetrating wounds may be quite stable as a result of the previously described retroperitoneal tamponade. Either compression with a finger or the direct application of vascular clamps can be used to control bleeding from a perforation of the renal vein. Lateral venorrhaphy remains the preferred technique of repair. If ligation of the right renal vein is necessary to control hemorrhage, nephrectomy should be performed either at the initial operation or at the reoperation if damage control has been necessary. The medial left renal vein, however, can be ligated as long as the left adrenal and gonadal veins are intact.128 Repair is preferable if feasible, as a greater frequency of postoperative renal complications has been noted in older series when ligation was performed.129 The survival rate for patients with penetrating injuries to the renal veins has ranged from 42% to 88% in the older literature, with the difference presumably due to the magnitude and number of associated visceral and vascular injuries.116,120,121 In three recent reviews, survival ranged from 44.2% to 70% with a mean of 60.4%.8,9,84
Injuries to the renal parenchyma are covered elsewhere.
MANAGEMENT OF INJURIES IN ZONE 3
Exposure and Vascular Control
The fourth major area of hematoma or hemorrhage is the pelvic retroperitoneum. In this location, the iliac artery, iliac vein, or both may be injured. The majority of injuries reported in major series are the result of penetrating trauma. It is of interest, however, that major blunt abdominal trauma or pelvic fractures, particularly of the open type, have, in the past 25 years, become a more frequent cause of occlusion or laceration of the iliac arteries than previously noted.20–22,130,131 In fact, a very recent study using the National Trauma Data Bank noted a 3.5% rate of blunt iliac artery injury in 6,377 patients with AIS 3 or 4 pelvic fracture.132 The presence of a blunt iliac arterial injury in combination with a pelvic fracture was associated with a significantly higher hospital mortality (40% vs. 15%) and was associated with a 7.7% amputation rate.132
If a hematoma or hemorrhage is present after penetrating trauma, compression with a laparotomy pad or finger or simply grabbing the bleeding vessels with a hand should be performed as proximal and distal vascular control is attained. The proximal common iliac arteries are exposed by eviscerating the small bowel to the right and dividing the midline retroperitoneum over the aortic bifurcation. In young trauma patients, there is usually no adherencebetween the common iliac artery and vein in this location, and vascular tapes can be passed rapidly around the proximal arteries. Distal vascular control is obtained at the point at which the external iliac artery comes out of the pelvis proximal to the inguinal ligament. The artery is readily palpable under the retroperitoneum and can be rapidly elevated into the field of view with a vascular tape. The major problem in this area is continued back-bleeding from the internal iliac artery. This artery can be exposed by further opening the retroperitoneum on the side of the pelvis, elevating the vascular tapes on the proximal common iliac and distal external iliac arteries, and looking for the large branch of the iliac artery that descends into the pelvis.
When bilateral iliac vascular injuries are present, one of the former coauthors of this chapter (Jon M. Burch) has used the technique of total pelvic vascular isolation. This includes proximal cross-clamping of the abdominal aorta and inferior vena cava just above their bifurcations and distal cross-clamping of both the external iliac artery and vein with one clamp on each side of the pelvis. Back-bleeding from the internal iliac vessels is minimal with this approach.
Injuries to the iliac veins are exposed through a technique similar to that described for injuries to the iliac arteries. It is not usually necessary to pass vascular tapes around these vessels, however, because they are readily compressible with either sponge sticks or fingers. As previously noted, the somewhat inaccessible location of the right common iliac vein has led to the suggested temporary transection of the right common iliac artery in order to improve exposure at this location.100 Similarly, transection and ligation of the internal iliac artery on the side of the pelvis will allow improved exposure of an injured ipsilateral internal iliac vein.133
Common, External, and Internal Iliac Arteries
Injuries to the common or external iliac artery should be repaired or temporarily shunted if at all possible. Ligation of either vessel in the hypotensive patient will lead to progressive ischemia of the lower extremity and the need for a high above-knee amputation or a hip disarticulation in the later postoperative course. In fact, in World War II, ligation of these vessels led to amputation rates of approximately 50%. Furthermore, in a large review by Burch et al. in the 1980s, mortality associated with ligation was 90%.134 In patients with severe shock, insertion of a temporary intraluminal shunt is a better choice for damage control.135 In contrast, an injured internal iliac artery can be ligated with impunity even with injuries that occur bilaterally.
Options in the management of more stable patients with injuries to the common or external iliac artery include the following: lateral arteriorrhaphy, completion of a partial transection and end-to-end anastomosis, resection of the injured area and insertion of a saphenous vein or PTFE graft,136,137 mobilization of the ipsilateral internal iliac artery to serve as a replacement for the external iliac artery, or transposition of one iliac artery to the side of the contralateral iliac artery for wounds at the bifurcation.138
Extensive injuries to the common or external iliac artery in the presence of significant enteric or fecal contamination in the pelvis remain a serious problem for the trauma surgeon. Both end-to-end repairs and vascular conduits in this location have suffered postoperative pseudoaneurysm formation and even blowouts secondary to pelvic infection from the original intestinal contamination. Therefore, the authors have occasionally avoided an end-to-end anastomosis or the insertion of a saphenous vein or PTFE graft in either the common or external iliac artery in such a situation. Rather, the artery is divided just proximal to the injury, closed with a double-running row of 4-0 or 5-0 polypropylene sutures, and covered with noninjured retroperitoneum or a vascularized pedicle of omentum. If the patient’s lower extremity on the side of the ligation appears to be in jeopardy at the completion of the abdominal operation, an extra-anatomic femorofemoral crossover graft should be performed to return arterial inflow to the extremity.23,73 If the surgeon chooses not to perform a femorofemoral crossover graft until the patient’s condition has been stabilized in the surgical intensive care unit, an ipsilateral four-compartment below-knee fasciotomy should be performed, since ischemic edema below the knee will often lead to a compartment syndrome.
The survival rate among patients with injuries to the iliac arteries will vary with the number of associated injuries to the iliac vein, aorta, and vena cava, but was approximately 61% in 189 patients reviewed in four large series published from 1981 to 1990 (Table 34-7).96,134,139,140 When patients with other vascular injuries, especially to the iliac vein, were eliminated, the survival rate among 57 patients in three series was 81% (Table 34-7).134,139,140 If the injury is large and free bleeding from the iliac artery into the peritoneal cavity has occurred during the preoperative period, the survival rate in one older series was only 45%.139
TABLE 34-7 Survival with Injuries to the Iliac Artery and Vein
The survival rates in two recent series for patients with injuries to the common iliac artery (other vascular injuries not specified) ranged from 44.7% to 55.5% with a mean of 46.8% (Table 34-7).9,84 In the same series the survival rate with injuries to the external iliac artery was a mean of 64.1% (Table 34-7).9,84 Finally, in another recent series, survival was correlated most heavily with preoperative base deficit, pH, and temperature. It was also noted that, even in busy trauma centers, significant delays to operative intervention occur, most notably prolonged emergency department time and anesthesia preparation times, and these delays adversely affected patient outcome.141 As such, every effort should be made to expedite operative intervention in a patient with a suspected abdominal vascular injury.
Blunt trauma to the iliac arteries is less common as they are protected by the bony pelvis and lie deep in the retroperitoneum. Partial transections, avulsions, and intimal injuries with secondary thrombosis have all been reported in association with pelvic fractures. Of the 10 patients with blunt thromboses reported in the literature until 1997, most had been treated with prosthetic interposition grafting, although several underwent primary repairs. Only one patient needed an amputation.131 As noted above, the recent study of patients in the National Trauma Data Bank documented a 7.7% amputation rate in patients with pelvic fractures and an associated injury to the iliac artery.132
Common, External, and Internal Iliac Veins
Injuries to the common or external iliac vein are treated either with lateral repair using 4-0 or 5-0 polypropylene suture or with ligation. Ligation in the young patient has been well tolerated in the authors’ experience and that of others if the same precautions used after ligation of the inferior vena cava are applied142; however, some centers strongly recommend repair rather than ligation for injuries of the common or external iliac veins.143 When significant narrowing of the common or external iliac vein results from a lateral repair, postoperative anticoagulation is appropriate to lessen the risk of thrombosis and/or pulmonary embolism.
The survival rate of patients with injuries to the iliac veins is variable, but was approximately 70% in 404 patients reviewed in five large series published from 1981 to 1990 (Table 34-7).96,134,139,140,144 When patients with other vascular injuries, especially to the iliac artery, were eliminated, the survival rate among 137 patients in three series was 95% (Table 34-7).134,139,140 The survival rate in three recent series in patients with injuries to the iliac vein (not otherwise specified or common/external/internal combined) was a mean of 65.1%.8,9,84
MANAGEMENT OF INJURIES IN THE PORTA HEPATIS
Exposure and Vascular Control
If a hematoma or hemorrhage is present in the area of the portal triad in the right upper quadrant, there may be injury to the portal vein, hepatic artery, or both. Furthermore, this vascular injury may be in combination with an injury to the common bile duct. When a hematoma is present, the proximal hepatoduodenal ligament should be looped with a vascular tape or a noncrushing vascular clamp should be applied (the Pringle maneuver) before the hematoma is entered. If hemorrhage is occurring, finger compression of the bleeding vessels will suffice until the vascular clamp is in place. The Pringle maneuver clamps the distal common bile duct as well as the bleeding vessels, but led to only one stricture of the common bile duct in one older series of hepatic injuries from the Ben Taub General Hospital in Houston, Texas.145 Because of the short length of the porta in many patients, it may be difficult to place a distal vascular clamp right at the edge of the liver. In such patients, manual compression with forceps may allow distal vascular control until the area of injury can be isolated. Because of the proximity of the common bile duct, no sutures should be placed into the porta until the vascular injury is precisely defined.
Injuries to the portal vein in the hepatoduodenal ligament are isolated in much the same fashion as injuries to the hepatic artery. The posterior position of the vein, however, makes the exposure of these injuries more difficult. Mobilization of the common bile duct to the left and of the cystic duct superiorly, coupled with an extensive Kocher maneuver, will usually allow for excellent visualization of any suprapancreatic injury after proximal (and, if possible, distal) vascular control has been obtained. As with proximal wounds to the superior mesenteric artery or vein, division of the neck of the pancreas is necessary on rare occasions to visualize perforations in the retropancreatic portion of the portal vein. With the assistant compressing the superior mesenteric vein below and a vascular clamp applied to the hepatoduodenal ligament above, the surgeon should open both ends of the retropancreatic tunnel over the anterior wall of the portal vein by gently spreading a clamp or scissors. This maneuver may be prevented above by the position of the gastroduodenal artery, which should then be divided and ligated. When the tips of the surgeon’s index fingers touch under the neck of the pancreas, two straight noncrushing intestinal (Glassman or Dennis) or slightly angled vascular (Glover) clamps are placed across the entire neck of the pancreas. The pancreas is divided between the clamps and retracted away until the perforations in the portal vein or proximal superior mesenteric or splenic veins are visualized.
Due to its short course, injury to any portion of the hepatic artery is rare. Replacement of the injured common hepatic artery with a substitute vascular conduit is rarely indicated, since most patients with a portal hematoma or hemorrhage also have significant injuries to the liver, right kidney, or inferior vena cava. As previously noted, ligation of the proper or common hepatic artery appears to be well tolerated in the young trauma patient, even when performed beyond the origin of the gastroduodenal artery, owing to the extensive collateral arterial flow to the liver.146–151 Because of the small size of the right or left hepatic artery, lateral repairs are often difficult and will frequently be followed by occlusion of the vessel in the postoperative period.
Because of its rarity, few large studies have been performed on injuries to the hepatic artery. A relatively large multicenter experience was published in 1995 by Jurkovich et al., which documented the course of 99 patients with injury to the portal triad. Of this group, 28 patients had 29 injuries to a segment of the hepatic artery. Nineteen patients underwent ligation with eight survivors (mortality 42%). Only one patient developed hepatic necrosis requiring debridement, and this patient had an associated extensive injury to that lobe. Seven patients had attempts at repair with only one survivor, and two other patients exsanguinated prior to therapy.151 It should be noted, again, that selective ligation of the right hepatic artery warrants a cholecystectomy. Fortunately, injuries to the hepatic artery remain rare, and survival rates in cases of such injury are usually related to the number and magnitude of associated injuries.
As noted above, injuries to any portion of the portal vein are more difficult to manage than are injuries to the hepatic artery, owing to the posterior location of the vein, the friability of its wall, and the greater blood flow through it. Techniques for repair of the vein are varied, but lateral venorrhaphy with a 4-0 or 5-0 polypropylene suture is preferred. More extensive maneuvers that have occasionally been used with success include the following: resection with an end-to-end anastomosis, interposition grafting, transposition of the splenic vein down to the superior mesenteric vein to replace the proximal portal vein, an end-to-side portacaval shunt, and a venovenous shunt from the superior mesenteric vein to the distal portal vein or inferior vena cava.81,98,117,152–155 Such vigorous attempts at restoration of blood flow have resulted from the concern about viability of the midgut if the portal vein is ligated. Unfortunately, any type of portal–systemic shunt may have the undesirable effect of causing hepatic encephalopathy, since the direction of splanchnic venous flow with the shunt would mimic that in the patient with cirrhosis and hepatofugal flow in the obstructed portal vein. Ligation of the vein is compatible with survival, as both Pachter et al.153 and Stone et al.98 have emphasized. In the 1979 review of the literature on this subject by Pachter et al., one of six survivors of ligation of the portal vein developed portal hypertension.153 The 1982 series by Stone et al. included 9 survivors among 18 patients who underwent ligation of the portal vein.98 In essence, ligation of the portal vein should be performed if an extensive injury is present and the patient is hypothermic, acidotic, and/or coagulopathic (damage control indicated). The surgeon must then be prepared to infuse significant amounts of fluids to reverse the transient peripheral hypovolemia secondary to splanchnic hypervolemia.98
To apply some perspective to the somewhat controversial area of injuries to the portal vein, a review of techniques for their management is helpful. The comprehensive older review by Graham et al. of 37 patients with injuries to the portal vein reported that 26 underwent lateral venorrhaphy, 5 had packing or clamping only, 4 (none of whom survived) had ligation, 1 had an end-to-end anastomosis, and 1 had a portacaval shunt.97 In contrast, the aforementioned review by Stone et al. of 46 patients included 17 who had lateral venorrhaphy, 18 who had ligation (9 survived), 7 in whom no repair was done, 3 who underwent an end-to-end anastomosis, and 1 who had a portacaval shunt.98Ivatury et al. have since reported on 14 patients with injuries to the portal vein, among whom exsanguination occurred in 3, venorrhaphy was performed in 10 (of whom 6 survived), and ligation was done in 1 (who survived).156Finally, Jurkovich reported on 56 injuries to the portal vein with 33 patients undergoing primary repair (42% mortality), 1 undergoing complex repair (died), and 10 undergoing ligation (90% mortality). An additional 11 patients died before therapy. This led to an overall survival rate of 36% compared with the 50% survival rate among 134 patients with injuries to the portal vein in six series from 1978 to 1987 (Table 34-8).81,96–98,154,156
TABLE 34-8 Survival with Injuries to the Portal Vein
Wounds of the retrohepatic and supradiaphragmatic vena cava are discussed elsewhere in this text.
INDICATIONS AND TECHNIQUES OF ENDOVASCULAR INTERVENTION IN ABDOMINAL VASCULAR INJURY
While patients with abdominal vascular injury who present with active hemorrhage generally require immediate open exploration, a smaller subset who present with contained hemorrhage or thrombosis may be candidates for endovascular techniques. While these techniques are now well accepted for contained disruptions of the thoracic aorta and have been very successful as an adjunct to nonoperative management of solid organ injuries, their role in true abdominal vascular injury is not as well established. Indeed, the literature describing endovascular techniques in these potentially devastating injuries is composed mostly of case reports and small case series, many of which are reviewed in the following sections.
Patients with injury to the intra-abdominal aorta, especially after penetrating trauma, often present with hemorrhagic shock from free intraperitoneal hemorrhage. Alternatively, they may present acutely or in a delayed fashion with thrombotic sequelae. First described by Campbell and Austin in 1969,157 “Seat belt aorta” describes acute aortic occlusion related to lap-belt injuries. While in the past, operative intervention has generally been the only option for definitive management, several endovascular techniques have recently been reported to address thrombotic complications of aortic injury in both the acute and chronic settings.
In 1997, Vernhet et al.158 described the management of three patients with acute infrarenal aortic dissection after trauma with percutaneous placement of a stent. These patients presented without obvious hemorrhagic shock and had varying degrees of arterial insufficiency. All were managed successfully in the early postinjury period with Wallstents (Schneider Wallstent, Schneider Stent Division, Pfizer, Minneapolis, Minnesota) used to cover their intimal injuries, obliterate the dissections, and restore perfusion. At 6-month to 2-year follow-up, no complications were noted.156 Other groups have presented similar case reports and case series, with successful use of stents to restore perfusion after blunt aortic injury.159,160
In recent years stent grafts have also been used to manage aortic trauma in both the acute setting and more chronic situations, especially in patients with missed injuries and “hostile” abdomens. Two groups have reported using stent grafts in a delayed fashion to manage abdominal aortic injury in patients with “hostile” abdomens from damage control laparotomy.161,162 In the first case report, a covered stent was placed in a patient with a contained zone 1 hematoma 6 days after a laparotomy after a motorcycle crash. At 24-month follow-up, no graft-related complications were noted.161 More recently, Yeh et al.162reported the use of a Zenith stent graft (Cook Group, Inc, Bloomington, Indiana) in a patient 2 weeks after laparotomy for multiple gunshot wounds to the torso. This patient presented with abrupt onset of hemorrhage and hemodynamic instability in the face of matted viscera and a hostile abdomen. Attempts at open repair failed, and the patient was packed and brought to the interventional suite where the stent graft was placed with successful cessation of hemorrhage. This patient survived a prolonged hospital course and was noted to have no aortic complications at a 1-year follow-up. Similarly, two case reports report the successful use of stent grafts in the management of traumatic aortocaval fistulas.163,164
Injuries to the inferior vena cava are generally the result of penetrating trauma and have been managed with many techniques including ligation in the infrarenal inferior vena cava as described above. In the last few years, several reports have described the use of interventional techniques to assist in the management of these complex injuries. Castelli et al.165 reported on a patient who presented with hemorrhagic shock 4 hours after a motor vehicle collision. CT angiography revealed an injury to the vena cava at the confluence of the iliac veins. In the interventional suite, a Gore Excluder stent graft was used (W.L. Gore, Flagstaff, Arizona) to control hemorrhage from the injury. The duration of the procedure was 9 minutes. Unfortunately, the patient died of a severe traumatic brain injury on post-trauma day 2. Two other case reports describe a similar management technique.166,167 Clearly, in the right institution, the technology is available to perform these procedures expeditiously, and this technique may benefit a small group of patients. One concern over placing stent grafts in the venous system is a question of durability and the ability to administer postoperative anticoagulation. Stent grafts are felt to be highly thrombogenic in the first month, and it is unknown whether their insertion in major venous structures will require routine postoperative anticoagulation. This may limit the use of this technique in the multiply injured patient.
As previously mentioned, injury to the main celiac axis is rare and, therefore, there have been no reports of the use of endovascular techniques for an injury to this vessel, although several authors have reported the use of endovascular techniques in the management of spontaneous celiac dissections and aneurysms.168 Whether this can be extrapolated to the trauma patient, most of whom are younger, healthier, and with longer life expectancy, is unknown. Branches of the celiac axis may be amenable to endovascular techniques. Splenic and hepatic artery injuries are covered elsewhere in this text. Successful embolization of a left gastric artery pseudoaneurysm after blunt abdominal trauma has been reported.169
Injury to the superior mesenteric artery is fortunately rare, with most cases being the result of penetrating trauma. Because most of these patients present with severe shock and there is a concomitant need to evaluate intestinal viability, endovascular management of traumatic injuries to the superior mesenteric artery has not been described and is likely unwise. This remains fundamentally different from patients with intestinal angina secondary to stenosis of their superior mesenteric artery or even atherosclerotic occlusion of the vessel, some of whom have been treated successfully with endovascular techniques.170
As previously mentioned, renovascular injuries are difficult to manage operatively, especially when the renal artery is involved. As the diagnosis is often somewhat delayed and because of the relatively poor function of kidneys revascularized with open surgery, enthusiasm for attempts at open repair has waned. Therefore, multiple authors have described endovascular management of injuries to the renal vasculature. Renal arteries and major branches have been embolized in series back into the 1980s with good renal preservation. For example, Sclafani and Becker171 reported on eight patients with renal injuries who were treated with angiographic embolization. The injuries were the result of stab wounds in five patients, blunt trauma in two patients, and a gunshot wound in one patient. Angiographic findings included two pseudoaneurysms, two arteriovenous fistulas, two arteriocalyceal fistulas, and one renal artery–pleural fistula. Of interest, seven of eight patients had successful procedures, and all seven had preservation of the kidney, with one nephrectomy performed for persistent hematuria. A more recent study revealed renal vascular injury in eight patients, of whom seven were successfully treated with angiographic embolization, obviating the need for open surgery. At discharge, all survivors had normal renal function and all patients were normotensive.172Thus, in the hemodynamically normal patient, transcatheter embolization has been used successfully to manage a variety of renovascular injuries and allow for organ preservation.
In more recent years with improving technology, there has been an increased interest in preserving blood flow to the renal parenchyma with the use of expandable stents rather than transcatheter embolization. At least three case reports document the successful use of various stents to obliterate intimal flaps in patients with renal artery injuries with preservation of renal function and no short-term complications.173–175
One of the earliest descriptions of endovascular management of traumatic aortoiliac disease was reported by Parodi et al. in 1993.176 Building on their experience with stent graft management of aortic aneurysmal disease, the management of arteriovenous fistulae in the iliac system was described in seven patients with up to 14-month follow-up and 100% technical success. In this study, PTFE grafts combined with Palmaz stents were used to repair the injured arterial wall under fluoroscopic guidance.176
In more recent years, several authors have reported on the use of stent grafts in traumatic iliac thrombosis. In 1997, Lyden et al.177 used a 10 × 60 mm Smart Stent (Cordis Endovascular, Miami, Florida) to manage a common iliac artery dissection and thrombosis after a motor vehicle collision. They were able to restore flow within 4 hours of injury, and while the patient had an excellent short-term result, he expired on hospital day 6 with a severe traumatic brain injury. Marin et al.178 also successfully managed several traumatic vascular injuries with stent grafts, including one injury to the common iliac artery, with patency documented at 2 months.
One of the largest series of nonthoracic vascular injuries managed with covered stents in the literature was published in 2006.179 In this multicenter trial, 62 patients were managed with Wallgraft endoprosthesis grafts over 6 years. This included 33 patients with injuries to the iliac vessels, most of which were iatrogenic in nature, and included 27 perforations, 4 arteriovenous fistulae, 1 pseudoaneurysm, and 1 dissection. Technical success, as defined by total postprocedure exclusion, was achieved in all but one patient with an injury to the iliac artery and primary patency at 1 year was 76% for these patients. Early adverse events occurred in 14% of patients, mostly related to puncture site complications, and a late adverse event occurred in another 6.5% of patients with one systemic infection, one occlusion, and three stenoses of the repair. All-cause mortality was 6.5% in the early postprocedure period and 17.7% in later follow-up. None of the deaths was thought to be the result of the stent graft.179
Therefore, in reviewing the literature on interventional techniques as a mode of therapy in traumatic iliac vascular injuries, one comes to the conclusion that improving technology and techniques may have an expanding role in the management of such injuries in the future. Unfortunately, long-term follow-up data are nonexistent and, therefore, it is unknown whether or not an endovascular prosthesis will be subject to the same risk of contamination and failure that has been seen with prosthetic material placed surgically.
The complications of vascular repairs in the abdomen are much the same as those seen in the extremities. They include such problems as thrombosis, dehiscence of a suture line, and infection.180 Occlusion is not uncommon when small, vasoconstricted vessels, such as the renal artery or superior mesenteric artery, undergo lateral arteriorrhaphy. In such patients, it may be valuable to perform a second-look operation within 12–24 hours after the patient’s temperature, coagulation abnormalities, and blood pressure have returned to normal. When this is done, correction of a vascular thrombosis may be successful.
Dehiscence of vascular suture lines in the abdomen occurred in two locations in the authors’ experience, and both have been previously discussed. First, a substitute vascular conduit inserted in the superior mesenteric artery near a pancreatic injury may be disrupted if a small pancreatic leak occurs in the postoperative period. For this reason, the proximal anastomosis of such a graft should be on the infrarenal abdominal aorta inferior to the transverse mesocolon and far away from the pancreas as previously noted. Second, the dehiscence of end-to-end anastomoses and conduit suture lines in the iliac arteries can be avoided by limiting the extent of repair if there is significant enteric or fecal contamination in the pelvis and considering early extra-anatomic bypass if the patient’s limb is threatened.
Finally, a vascular complication unique to the abdomen is the postoperative development of vascular–enteric fistulas. This will occur most commonly in patients who have anterior aortic repairs, aortic grafts, or grafts to the superior mesenteric artery from the aorta. Again, this problem can be avoided by proper coverage of suture lines on the aorta with retroperitoneal tissue or a viable omental pedicle106 and on the recipient vessel with mesentery.
Abdominal vascular injuries are commonly seen in patients with penetrating wounds to the abdomen (Figs. 34-6 and 34-7). They present either with a contained retroperitoneal, mesenteric, or portal hematoma or with active hemorrhage. When tamponade is present, proximal and distal vascular control should be obtained before opening the hematoma causing the tamponade. If active hemorrhage is present, direct compression of the bleeding vessels with a finger, hand, laparotomy pad, or sponge stick at the site of injury is necessary until proximal and distal vascular control can be attained. Vascular repairs are generally performed with polypropylene sutures and can range from simple arteriorrhaphy or venorrhaphy to the insertion of substitute vascular conduits, much as in vascular injuries in the extremities. Also, in the occasional patient who presents with normal hemodynamics, thrombotic sequelae, or in a delayed fashion after abdominal vascular injury, endovascular techniques may have a role in management. Overall, if hemorrhage can be rapidly controlled and distal perfusion restored, many patients with major abdominal vascular injuries can be salvaged with the techniques described in this chapter.
FIGURE 34-6 Blunt abdominal vascular injury algorithm.
FIGURE 34-7 Penetrating abdominal vascular injury algorithm.
1. DeBakey ME, Simeone FA. Battle injuries of the arteries in World War II: an analysis of 2,471 cases. Ann Surg. 1946;123:534.
2. Hughes CW. Arterial repair during the Korean War. Ann Surg. 1958;147:555.
3. Rich NM, Baugh JH, Hughes CW. Acute arterial injuries in Vietnam: 1,000 cases. J Trauma. 1970;10:359.
4. Beekley AC, Blackbourne LH, Sebesta JA, et al. Selective nonoperative management of penetrating injury from combat fragmentation wounds. J Trauma. 2008;64:S108.
5. Rapaport A, Feliciano DV, Mattox KL. An epidemiologic profile of urban trauma in America—Houston style. Tex Med. 1982;78:44.
6. Feliciano DV, Bitondo CG, Mattox KL, et al. Civilian trauma in the 1980’s. A 1-year experience with 456 vascular and cardiac injuries. Ann Surg. 1984;199:717.
7. Mattox KL, Feliciano DV, Burch J, et al. Five thousand seven hundred sixty cardiovascular injuries in 4459 patients. Epidemiologic evolution 1958 to 1987. Ann Surg. 1989;209:698.
8. Asensio JA, Chahwan S, Hanpeter D, et al. Operative management and outcome of 302 abdominal vascular injuries. Am J Surg. 2001;180:528.
9. Davis TP, Feliciano DV, Rozycki GS, et al. Results with abdominal vascular trauma in the modern era. Am Surg. 2001;67:565.
10. Kelly JF, Ritenour AE, McLaughlin DF, et al. Injury severity and causes of death from Operation Iraqi Freedom and Operation Enduring Freedom: 2003–2004 versus 2006. J Trauma. 2008;64:S21.
11. Fischer RP, Miller-Crotchett P, Reed RL II. Gastrointestinal disruption: the hazard of nonoperative management in adults with blunt abdominal injury. J Trauma. 1988;28:1445.
12. Cox CF. Blunt abdominal trauma. A 5-year analysis of 870 patients requiring celiotomy. Ann Surg. 1984;199:467.
13. Feliciano DV, Burch JM, Spjut-Patrinely V, et al. Abdominal gunshot wounds: an urban trauma center’s experience with 300 consecutive patients. Ann Surg. 1988;208:362.
14. Swana HS, Cohn SM, Burns GA, Egglin TK. Renal artery pseudoaneurysm after blunt abdominal trauma: case report and literature review. J Trauma. 1996;40:459.
15. Jebara VA, El Rassi I, Achouh PE, et al. Renal artery pseudoaneurysm after blunt abdominal trauma. J Vasc Surg. 1998;27:362.
16. Haas CA, Dinchman KH, Nasrallah PF, et al. Traumatic renal artery occlusion: a 15-year review. J Trauma. 1998;45:557.
17. Pezzella AT, Griffen WO Jr, Ernst CB. Superior mesenteric artery injury following blunt abdominal trauma: case report with successful primary repair. J Trauma. 1978;18:472.
18. Michaels AJ, Gerndt SJ, Taheri PA, et al. Blunt force injury of the abdominal aorta. J Trauma. 1996;41:105.
19. Siavelis HA, Mansour MA. Aortoiliac dissection after blunt abdominal trauma: case report. J Trauma. 1997;43:862.
20. Nitecki S, Karmeli R, Ben-Arien Y, et al. Seatbelt injury to the common iliac artery: report of two cases and review of the literature. J Trauma. 1992;33:935.
21. Buscaglia LC, Matolo N, Macbeth A. Common iliac artery injury from blunt trauma: case reports. J Trauma. 1989;29:697.
22. Roth SM, Wheeler JR, Gregory RT, et al. Blunt injury of the abdominal aorta: a review. J Trauma. 1997;42:748.
23. Feliciano DV. Abdominal vascular injuries. Surg Clin North Am. 1988;68:741.
24. Courcy PA, Brotman S, Oster-Granite ML, et al. Superior mesenteric artery and vein injuries from blunt abdominal trauma. J Trauma. 1984; 24:843.
25. Matsubara J, Seko T, Ohta T, et al. Traumatic aneurysm of the abdominal aorta with acute thrombosis of bilateral iliac arteries. Arch Surg. 1983;118:1337.
26. Bass A, Papa M, Morag B, et al. Aortic false aneurysm following blunt trauma of the abdomen. J Trauma. 1983;23:1072.
27. Feliciano DV. Pitfalls in the management of peripheral vascular injuries. Probl Gen Surg. 1986;3:101.
28. Rich NM, Hobson RW II, Fedde CW. Vascular trauma secondary to diagnostic and therapeutic procedures. Am J Surg. 1974;128:715.
29. McDonald PT, Rich NM, Collins GJ Jr, et al. Vascular trauma secondary to diagnostic and therapeutic procedures: laparoscopy. Am J Surg. 1978;135:651.
30. Kozloff L, Rich NM, Brott WH, et al. Vascular trauma secondary to diagnostic and therapeutic procedures: cardiopulmonary bypass and intraaortic balloon assist. Am J Surg. 1980;140:302.
31. Ingram WL, Feliciano DV, Renz BM, et al. Blood pressure in the emergency department in patients with abdominal vascular injuries: effect on management and prognostic valve. Presented at: 55th Annual Meeting of the American Association for the Surgery of Trauma; September 27–30, 1995; Halifax, Nova Scotia, Canada.
32. Eachempati SR, Robb T, Ivatury RR, et al. Factors associated with mortality in patients with penetrating abdominal vascular trauma. J Surg Res. 2002;108:222.
33. Rozycki GS, Feliciano DV, Schmidt, JA, et al. The role of surgeon-performed ultrasound in patients with possible cardiac wounds. Ann Surg. 1996;223:737.
34. Sisley AC, Rozycki GS, Ballard RB, et al. Rapid detection of traumatic effusion using surgeon-performed ultrasonography. J Trauma. 1998;44:291.
35. Rozycki GS, Ballard RB, Feliciano DV, et al. Surgeon-performed ultrasound for the assessment of truncal injuries. Lessons learned from 1540 patients. Ann Surg. 1998;228:557.
36. Rozycki GS, Cava RA, Tchorz KM. Surgeon-performed ultrasound imaging in acute surgical disorders. Curr Probl Surg. 2001;38:141.
37. Sclafani SJA. The diagnosis of bilateral renal artery injury by computed tomography. J Trauma. 1986;26:295.
38. Nagy KK, Brenneman FD, Krosner SM, et al. Routine preoperative “one-shot” intravenous pyelography is not indicated in all patients with penetrating abdominal trauma. J Am Coll Surg. 1997;185:530.
39. Panetta T, Sclafani SJA, Goldstein AS, et al. Percutaneous transcatheter embolization for massive bleeding from pelvic fractures. J Trauma. 1985;25:1021.
40. Daly KP, Ho CP, Persson DL, et al. Traumatic retroperitoneal injuries: review of multidetector CT findings. Radiographics. 2008;28:1571.
41. Seamon MJ, Smoyer D, Torres DM, et al. A prospective validation of a current practice: the detection of extremity vascular injury with CT-angiography. J Trauma. 2009;67:238.
42. Maturen KE, Adusumilli S, Blane CE, et al. Contrast-enhanced CT accurately detects hemorrhage in torso trauma: direct comparison with angiography. J Trauma. 2007;62:740.
43. Chesnut RM. Avoidance of hypotension: conditio sine qua non of successful severe head-injury management. J Trauma. 1997;42:S4.
44. Kaweski SM, Sise MJ, Virgilio RW. The effect of prehospital fluids on survival in trauma. J Trauma. 1990;30:1215.
45. Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331:1105.
46. Beekley AC. Damage control resuscitation: a sensible approach to the exsanguinating surgical patient. Crit Care Med. 2008;36:S267.
47. Feliciano DV, Bitondo CG, Cruse PA, et al. Liberal use of emergency center thoracotomy. Am J Surg. 1986;152:654.
48. Asensio JA, Wall M, Minei J, et al. Practice management guidelines for emergency department thoracotomy. J Am Coll Surg. 2001;193:303.
49. Dutky PA, Stevens SL, Maull KI. Factors affecting rapid fluid resuscitation with large-bore introducer catheters. J Trauma. 1989;29:856.
50. Gentilello LM. Practical approaches to hypothermia. In: Maull KI, Cleveland HC, Feliciano DV, et al., eds. Advances in Trauma Critical Care. Vol. 9. St. Louis: Mosby; 1994:39.
51. Rotondo MF, Schwab CW, McGonigal GR III, et al. “Damage control”: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. 1993;35:375.
52. Cotton BA, Gunter OL, Isbell J, et al. Damage control hematology: the impact of a trauma exsanguination protocol on survival and blood product utilization. J Trauma. 2008;64:1177.
53. Kashuk JL, Moore EE, Johnson JL, et al. Postinjury life threatening coagulopathy: is 1:1 fresh frozen plasma:packed red blood cells the answer? J Trauma. 2008;65:261.
54. Dente CJ, Shaz BH, Nicholas JM, et al. Improvement in early mortality and coagulopathy are sustained better in patients with blunt trauma after institution of a massive transfusion protocol in a civilian level I trauma center. J Trauma. 2009;66:1616.
55. Moore FA, Nelson T, McKinley BA, et al. Is there a role for aggressive use of fresh frozen plasma in massive transfusion of civilian trauma patients? Am J Surg. 2008;196:948.
56. Feliciano DV, Rozycki GS. The management of penetrating abdominal trauma. In: Cameron JL, ed. Advances in Surgery. Vol. 28. St. Louis: Mosby; 1995:1.
57. Samkaran S, Lucas C, Walt AJ. Thoracic aortic clamping for prophylaxis against sudden cardiac arrest during laparotomy for acute massive hemoperitoneum. J Trauma. 1975;15:290.
58. Ledgerwood AM, Kazmers M, Lucas CE. The role of thoracic aortic occlusion for massive hemoperitoneum. J Trauma. 1976;16:610.
59. Wiencek RG Jr, Wilson RF. Injuries to the abdominal vascular system: how much does aggressive resuscitation and prelaparotomy thoracotomy really help? Surgery. 1987;102:731.
60. Accola KD, Feliciano DV, Mattox KL, et al. Management of injuries to the superior mesenteric artery. J Trauma. 1986;26:313.
61. Henry SM, Duncan AO, Scalea TM. Intestinal Allis clamps as temporary vascular control for major retroperitoneal venous injury. J Trauma. 2001;51:170.
62. Moore EE, Cogbill TH, Jurkovich GJ, et al. Organ injury scaling III: chest wall, abdominal vascular, ureter, bladder, and urethra. J Trauma. 1992;33:337.
63. DeBakey ME, Creech O Jr, Morris GC Jr. Aneurysm of thoracoabdominal aorta involving the celiac superior mesenteric and renal arteries. Report of four cases treated by resection and homograft replacement. Ann Surg. 1956;144:549.
64. Elkins RC, DeMeester TR, Brawley RK. Surgical exposure of the upper abdominal aorta and its branches. Surgery. 1971;70:622.
65. Mattox KL, McCollum WB, Jordan GL Jr, et al. Management of upper abdominal vascular trauma. Am J Surg. 1974;128:823.
66. Fry WR, Fry RE, Fry WJ. Operative exposure of the abdominal arteries for trauma. Arch Surg. 1991;126:289.
67. Feliciano DV. Injuries to great vessels of the abdomen. In: Holcroft JW, ed. Scientific American Surgery. Trauma Section. New York: Scientific American; 1998:1:chap 9, section 4.
68. Conn J Jr, Trippel OH, Bergan JJ. A new atraumatic aortic occluder. Surgery. 1968;64:1158.
69. Mahoney BD, Gerdes D, Roller B, et al. Aortic compressor for aortic occlusion in hemorrhagic shock. Ann Emerg Med. 1984;13:29.
70. Veith FJ, Gupta S, Daly V. Technique for occluding the supraceliac aorta through the abdomen. Surg Gynecol Obstet. 1980;151:426.
71. Illig KA, Green RM, Ouriel K, et al. Primary fibrinolysis during supraceliac aortic clamping. J Vasc Surg. 1997;25:244.
72. Kavic SM, Atweb N, Ivy ME, et al. Celiac axis ligation after gunshot wound to the abdomen: case report and literature review. J Trauma. 2001;50:738.
73. Feliciano DV. Approach to major abdominal vascular injury. J Vasc Surg. 1988;7:730.
74. Farret A, da Ros CT, Fischer CAC, et al. Suprarenal aorta reconstruction using saphenous spiral graft: case report. J Trauma. 1994;37:144.
75. Accola KD, Feliciano DV, Mattox KL, et al. Management of injuries to the suprarenal aorta. Am J Surg. 1987;154:613.
76. Oyama M, McNamara JJ, Suehiro GT, et al. The effects of thoracic aortic cross-clamping and declamping on visceral organ blood flow. Ann Surg. 1983;197:459.
77. Dente CJ, Wyryzkowski AD, Feliciano DV. Fasciotomy. Curr Probl Surg. 2009;46:769.
78. Lim RC Jr, Trunkey DD, Blaisdell FW. Acute abdominal aortic injury. An analysis of operative and postoperative management. Arch Surg. 1974;109:706.
79. Buchness MP, LoGerfo FW, Mason GR. Gunshot wounds of the suprarenal abdominal aorta. Ann Surg. 1976;42:1.
80. Brinton M, Miller SE, Lim RC Jr, et al. Acute abdominal aortic injuries. J Trauma. 1982;22:481.
81. Kashuk JL, Moore EE, Millikan JS, et al. Major abdominal vascular trauma—a unified approach. J Trauma. 1982;22:672.
82. Millikan JS, Moore EE. Critical factors in determining mortality from abdominal aortic trauma. Surg Gynecol Obstet. 1985;160:313.
83. Jackson MR, Olson DW, Beckett WC, et al. Abdominal vascular trauma. Am Surg. 1992;58:622.
84. Tyburski JG, Wilson RF, Dente C, et al. Factors affecting mortality rates in patients with abdominal vascular injuries. J Trauma. 2001;50:1020.
85. Coimbra R, Hoyt D, Winchell R, et al. The ongoing challenge of retroperitoneal vascular injuries. Am J Surg. 1996;172:541.
86. Asensio JA, Petrone P, Kimbrell B, et al. Lessons learned in the management of thirteen celiac axis injuries. South Med J. 2005;98:462.
87. Schreiber JP, Fritz Angle, J, Matsumoto AH, et al. Acute visceral ischemia occurring subsequent to blunt abdominal trauma: potential culpability of median arcuate ligament compression. J Trauma. 1998;45:404.
88. Fullen WD, Hunt J, Altemeier WA. The clinical spectrum of penetrating injury to the superior mesenteric arterial circulation. J Trauma. 1972;12:656.
89. Asensio JA, Britt LD, Borzotta A, et al. Multiinstitutional experience with the management of superior mesenteric artery injuries. J Am Coll Surg. 2001;193:354.
90. Ledgerwood A, Lucas CE. Survival following proximal superior mesenteric artery occlusion from trauma. J Trauma. 1974;14:622.
91. Reilly PM, Rotondo MF, Carpenter JP, et al. Temporary vascular continuity during damage control: intraluminal shunting for proximal superior mesenteric artery injury. J Trauma. 1995;39:757.
92. Nolan BW, Gabram SG, Schwartz RJ, et al. Mesenteric injury from blunt abdominal trauma. Am Surg. 195;61:501.
93. Pennington CJ, Gwaltney N, Sweitzer D. Microvascular repair of jejunal and ileal vessels for near complete mesenteric avulsion after seat-belt injury. J Trauma. 2000;48:327.
94. Graham JM, Mattox KL, Beall AC Jr, et al. Injuries to the visceral arteries. Surgery. 1978;84:835.
95. Lucas AE, Richardson JD, Flint LM, et al. Traumatic injury of the proximal superior mesenteric artery. Ann Surg. 1981;193:30.
96. Sirinek KR, Gaskill HV III, Root HD, et al. Truncal vascular injury—factors influencing survival. J Trauma. 1983;23:372.
97. Graham JM, Mattox KL, Beall AC Jr. Portal venous system injuries. J Trauma. 1978;18:419.
98. Stone HH, Fabian TC, Turkleson ML. Wounds of the portal venous system. World J Surg. 1982;6:335.
99. Donahue TK, Strauch GO. Ligation as definitive management of injury to the superior mesenteric vein. J Trauma. 1988;28:541.
100. Salam AA, Stewart MT. New approach to wounds of the aortic bifurcation and inferior vena cava. Surgery. 1985;98:105.
101. Burch JM, Feliciano DV, Mattox KL, et al. Injuries of the inferior vena cava. Am J Surg. 1988;156:548.
102. Ravikumar S, Stahl WM. Intraluminal balloon catheter occlusion for major vena cava injuries. J Trauma. 1985;25:458.
103. Linker RW, Crawford FA Jr, Rittenbury MS, et al. Traumatic aortocaval fistula: case report. J Trauma. 1989;29:255.
104. Feliciano DV, Burch JM, Mattox KL, et al. Balloon catheter tamponade in cardiovascular wounds. Am J Surg. 1990;160:583.
105. Ball CG, Wyrzykowski AD, Nicholas JM, et al. A decade’s experience with balloon catheter tamponade for the emergency control of hemorrhage. J Trauma. 2011;70:330.
106. Bunt TJ, Doerhoff CR, Haynes JL. Retrocolic omental pedicle flap for routine plication of abdominal aortic grafts. Surg Gynecol Obstet. 1984;158:591.
107. Munez AE, Haynes JH. Delayed abdominal aortic rupture in a child with a seat-belt sign and review of the literature. J Trauma. 2004;56:194.
108. Cheek RC, Pope JC, Smith HF, et al. Diagnosis and management of major vascular injuries: a review of 200 operative cases. Am Surg. 1975;41:755.
109. Carrillo EH, Ginzburg E, Namias N, et al. Spontaneous rupture of abdominal aortic aneurysms in patients with non-related blunt traumatic injuries. Ky Med. 1997;15:64.
110. Ali MR Jr, Norcross ED, Brothers TE. Iliac and femoral artery occlusion by thromboemboli from an abdominal aortic aneurysm in the setting of blunt abdominal trauma. J Vasc Surg. 1998;27:545.
111. Sullivan PS, Dente CJ, Patel S, et al. Outcome of ligation of the inferior vena cava in the modern era. Am J Surg. 2010;199:500.
112. Nigro J, Velmahos GC. Delayed reconstruction of the inferior vena cava with prosthetic graft due to postligation edema. Contemp Surg. 1999; 54:25.
113. Ivy ME, Possenti P, Atweh N, et al. Ligation of the suprarenal vena cava after a gunshot wound. J Trauma. 1998;45:630.
114. Oldhafer KJ, Frerker M, Winkler M, et al. Complex inferior vena cava and renal vein reconstruction after abdominal gunshot injury. J Trauma. 1999;46:721.
115. Graham JM, Mattox KL, Beall AC Jr. Traumatic injuries of the inferior vena cava. Arch Surg. 1978;113:413.
116. Kudsk KA, Bongard F, Lim RC Jr. Determinants of survival after vena caval injury: analysis of a 14-year experience. Arch Surg. 1984; 119:1009.
117. Wiencek RG, Wilson RF. Abdominal venous injuries. J Trauma. 1986;26:771.
118. Klein SR, Baumgartner FJ, Bongard FS. Contemporary management strategy for major inferior vena caval injuries. J Trauma. 1994;37:35.
119. Porter JM, Ivatury RR, Islam SZ, et al. Inferior vena cava injuries: noninvasive follow-up of venorrhaphy. J Trauma. 1997;42:913.
120. McAninch JW, Carroll PR. Renal trauma: kidney preservation through improved vascular control. J Trauma. 1985;22:285.
121. Carroll PR, McAninch JW, Klosterman P, Greenblatt M. Renovascular trauma: risk assessment, surgical management, and outcome. J Trauma. 1990;30:547.
122. Gonzalez RP, Falimirski M, Holevar MR, et al. Surgical management of renal trauma: is vascular control necessary? J Trauma. 1999; 47:1039.
123. Barone GW, Kahn MB, Cook JM, et al. Traumatic left renal artery stenosis managed with splenorenal bypass: case report. J Trauma. 1990; 30:1594.
124. Brown MF, Graham JM, Mattox KL, et al. Renovascular trauma. Am J Surg. 1980;140:802.
125. Maggio AJ Jr, Brosman S. Renal artery trauma. Urology. 1978;11:125.
126. Frassinelli P, Pasquale MD, Reckard C, et al. Bilateral renal artery thrombosis secondary to blunt trauma: case report and review of the literature. J Trauma. 1997;42:330.
127. Greenholz SK, Moore EE, Peterson NE, et al. Traumatic bilateral renal artery occlusion: successful outcome without surgical intervention. J Trauma. 1986;26:941.
128. James EC, Fedde CW, Khuri NT, et al. Division of the left renal vein: a safe surgical adjunct. Surgery. 1978;83:151.
129. Rastad J, Almgren B, Bowald S, et al. Renal complications to left renal vein ligation in abdominal aortic surgery. J Cardiovasc Surg. 1984; 25:432.
130. Rothenberger DA, Fischer RP, Perry JF Jr. Major vascular injuries secondary to pelvic fractures: an unsolved clinical problem. Am J Surg. 1978;136:660.
131. Tsai FC, Wang CC, Fang JF, et al. Isolated common iliac artery occlusion secondary to atherosclerotic plaque rupture from blunt abdominal trauma: case report and review of the literature. J Trauma. 1997; 42:133.
132. Cestero RF, Plurad D, Green D, et al. Iliac artery injuries and pelvic fracture: a National Trauma Database analysis of associated injuries and outcomes. J Trauma. 2009;67:715.
133. Vitelli CE, Scalea TM, Phillips TF, et al. A technique for controlling injuries of the iliac vein in the patient with trauma. Surg Gynecol Obstet. 1988;166:551.
134. Burch JM, Richardson RJ, Martin RR, Mattox KL. Penetrating iliac vascular injuries: experience with 233 consecutive patients. J Trauma. 1990;30:1450.
135. Ball CG, Feliciano DV. Damage control techniques for common and external iliac artery injuries: have temporary intravascular shunts replaced the need for ligation? J Trauma. 2010;68:1117.
136. Feliciano DV, Mattox KL, Graham JM, et al. Five-year experience with PTFE grafts in vascular wounds. J Trauma. 1985;25:71.
137. Landercasper RJ, Lewis DM, Snyder WH. Complex iliac arterial trauma: autologous or prosthetic vascular repair. Surgery. 1993;114:9.
138. Landreneau RJ, Mitchum P, Fry WJ. Iliac artery transposition. Arch Surg. 1989;124:978.
139. Millikan JS, Moore EE, Van Way CW III, et al. Vascular trauma in the groin: contrast between iliac and femoral injuries. Am J Surg. 1981; 142:695.
140. Ryan W, Snyder W III, Bell T, et al. Penetrating injuries of the iliac vessels. Am J Surg. 1982;144:642.
141. Cushman JG, Feliciano DV, Renz BM, et al. Iliac vessel injury: operative physiology related to outcome. J Trauma. 1997;42:1033.
142. Mullins RJ, Lucas CE, Ledgerwood AM. The natural history following venous ligation for civilian injuries. J Trauma. 1980;20:737.
143. Agarwal N, Shah PM, Clauss RH, et al. Experience with 115 civilian venous injuries. J Trauma. 1982;22:827.
144. Wilson RF, Wiencek RG, Balog M. Factors affecting mortality rate with iliac vein injuries. J Trauma. 1990;30:320.
145. Feliciano DV, Mattox KL, Jordan GL Jr, et al. Management of 1000 consecutive cases of hepatic trauma (1979–1984). Ann Surg. 1986; 204:438.
146. Mays ET, Wheeler CS. Demonstration of collateral arterial flow after interruption of hepatic arteries in man. N Engl J Med. 1974; 290:993.
147. Mays ET, Conti S, Fallahzadeh H, et al. Hepatic artery ligation. Surgery. 1979;86:536.
148. Flint LM Jr, Polk HC Jr. Selective hepatic artery ligation: limitations and failures. J Trauma. 1979;19:319.
149. Bryant DP, Cooney RN, Smith JS, et al. Traumatic proper hepatic artery occlusion: case report. J Trauma. 2001;50:735.
150. Graham DD, May AK, Moore M, et al. Management of hepatic artery injury: case report. Am Surg. 1997;63:327.
151. Jurkovich GJ, Hoyt DB, Moore FA, et al. Portal triad injuries. J Trauma. 1995;39:426.
152. Busuttil RW, Storm FK, Wilbur BG, et al. Use of the splenic vein in the reconstruction of portal and superior mesenteric veins after traumatic injury. Surg Gynecol Obstet. 1977;145:591.
153. Pachter HL, Drager S, Godfrey N, et al. Traumatic injuries of the portal vein. Ann Surg. 1979;189:383.
154. Petersen SR, Sheldon GF, Lim RC Jr. Management of portal vein injuries. J Trauma. 1979;19:616.
155. Busuttil RW, Kitahama A, Cerise E, et al. Management of blunt and penetrating injuries to the porta hepatis. Ann Surg. 1980;191:641.
156. Ivatury RR, Nallathambi M, Lankin DH, et al. Portal vein injuries. Noninvasive follow-up of venorrhaphy. Ann Surg. 1987;206:733.
157. Campbell DK, Austin RF. Acute occlusion of the infrarenal aorta from blunt trauma. Radiology. 1969;92:123.
158. Vernhet H, Marty-Ane CH, Lesnik A, et al. Dissection of the abdominal aorta in blunt trauma: management by percutaneous stent placement. Cardiovasc Intervent Radiol. 1997;20:473.
159. Berthet JP, Marty-Ane CH, Veerapen R, et al. Dissection of the abdominal aorta in blunt trauma: endovascular or conventional surgical management? J Vasc Surg. 2003;38:997.
160. Picard E, Marty-Ane CH, Vernhet H, et al. Endovascular management of traumatic infrarenal abdominal aortic dissection. Ann Vasc Surg. 1998;12:515.
161. Scharrer-Pamler R, Gorich J, Orend KH, et al. Emergent endoluminal repair of delayed abdominal aortic rupture after blunt trauma. J Endovasc Surg. 1998;5:134.
162. Yeh MW, Horn JK, Schecter WP, et al. Endovascular repair of an actively hemorrhaging gunshot injury to the abdominal aorta. J Vasc Surg. 2005;42:1007.
163. Tucker S Jr, Rowe VL, Rao R, et al. Treatment options for traumatic pseudoaneurysms of the paravisceral abdominal aorta. Ann Vasc Surg. 2003;19(5):613.
164. Waldrop JL, Dart BW IV, Barker DE. Endovascular stent graft treatment of traumatic aortocaval fistula. Ann Vasc Surg. 2005;19:562.
165. Castelli P, Caronno R, Piffaretti G, et al. Emergency endovascular repair for traumatic injury of the inferior vena cava. Eur J Cardiothorac Surg. 2005;28:906.
166. Erzurum VZ, Shoup M, Borge M, et al. Inferior vena cava endograft to control surgically inaccessible hemorrhage. J Vasc Surg. 2003;38:1437.
167. Watarida S, Nishi T, Furukawa A, et al. Fenestrated stent-graft for traumatic juxtahepatic inferior vena cava injury. J Endovasc Ther. 2002;9:134.
168. Edwards MS, Cherr GS, Craven TE, et al. Management of aneurysms involving branches of the celiac and superior mesenteric arteries: a comparison of surgical and endovascular therapy. J Vasc Surg. 2006;44:718.
169. Varela JE, Salzman SL, Owens C, et al. Angiographic embolization of a left gastric artery pseudoaneurysm after blunt abdominal trauma. J Trauma. 2006;60:1350.
170. Acosta S, Sonesson B, Resch T. Endovascular therapeutic approach for acute superior mesenteric artery occlusion. Cardiovasc Intervent Radiol. 2009;32:896.
171. Sclafani SJA, Becker JA. Interventional radiology in the treatment of retroperitoneal trauma. Urol Radiol. 1985;7:219.
172. Hagiwara A, Sakaki S, Goto H, et al. The role of interventional radiology in the management of blunt renal injury: a practical protocol. J Trauma. 2001;3:526.
173. Whigham CJ, Bodenhamer JR, Miller JK. Use of the Palmaz stent in primary treatment of renal artery intimal injury secondary to blunt trauma. J Vasc Interv Radiol. 1995;2:175.
174. Lee JT, White RA. Endovascular management of blunt traumatic renal artery dissection. J Endovasc Ther. 2002;9:354.
175. Villas PA, Cohen G, Putnam SG. Wallstent placement in a renal artery after blunt trauma. J Trauma. 1999;46:1137.
176. Parodi JC, Barone HD, Schonholz C. Transfemoral endovascular treatment of aortoiliac aneurysms and arteriovenous fistulas with stented Dacron grafts. In: Vejth FJ, ed. Current Critical Problems in Vascular Surgery. St. Louis, MO: Quality Medical Publishing; 1993:264.
177. Lyden SP, Srivastava SD, Wadlman DL, et al. Common iliac artery dissection after blunt trauma: case report of endovascular repair and literature review. J Trauma. 2001;50:339.
178. Marin ML, Veith FJ, Panetta TF, et al. Transluminally placed endovascular stented graft repair for arterial trauma. J Vasc Surg. 1994;20:466.
179. White R, Krajcer Z, Johnson M, et al. Results of a multicenter trial for the treatment of traumatic vascular injury with a covered stent. J Trauma. 2006;60:1189.
180. Feliciano DV. Management of infected grafts and graft blowout in vascular trauma patients. In: Flanigan DP, Schuler JJ, Meyer JP, eds. Civilian Vascular Trauma. Philadelphia, PA: Lea & Febiger; 1992:447.