Key Words:
inferior vena cava (IVC) , portal vein , mesenteric veins , venous trauma , noncompressible hemorrhage
Introduction
Injury to a major vein of the abdomen is highly lethal, thus accounting for limited operative experience. The current literature consistently describes mortality rates of 50% to 70% for injuries to the superior mesenteric vein (SMV), the portal vein (PV), and the inferior vena cava (IVC). With IVC injuries alone, 30% to 50% of patients will not survive to hospital arrival. These arresting mortality figures have been attributed to factors including difficulty in operatively accessing the structures, both for exposure of the vessel and for proximal and distal control, as well as torrential hemorrhage from a high-flow, low-pressure system. Low incidence renders few trauma surgeons greatly experienced in their management and limits the opportunity for study. Despite modern advances in patient transport, hemorrhage control, operative management, and intensive care unit (ICU) care, mortality rates for this series of injuries have remained fixed.
Historical Background
The infrequency of these injuries is reinforced in the historical literature. Reviews of combat injuries from World War I through the Korean War mention a variety of vascular injuries but contain little reference to either venous or arterial abdominal vascular injuries. One of the few references, from DeBakey and Simeone, mentions 2% of 2471 vascular injuries from WWII were intraabdominal. Three decades later, an oblique reference from the Walter Reed vascular registry documented lower extremity edema as a sequela of injuries to the vena cava managed by ligation. The Baylor group has published some of the most comprehensive reviews of visceral vascular injuries among civilian populations. In a 1982 review of 312 patients with vascular injury, venous injuries most commonly occurred to the internal jugular vein (5.7% of vascular injuries), with the SMV injured 2% of the time and the inferior mesenteric vein (IMV) injured in 0.4% of patients. An additional review of 4459 patients over a 30-year period found 33.7% were to the abdominal vasculature and 3.8% were to the mesenteric vessels.
The mortality associated with this triad of abdominal venous injuries has changed little in the last 30 years, despite advances in other areas of trauma care. Though comprehensive reviews are uncommon, case reports of heroic efforts to save patients using highly specialized management options are abundant. Approaches describing the role of interventional vascular techniques in hemorrhage control and repair are becoming increasingly common. The military experience with vascular shunts provides a unique opportunity to expose injuries and to resuscitate patients in relatively bloodless fields. While aggressive options such as venovenous bypass and liver explantation are largely anecdotal, they may provide future opportunities to repair the most profound injuries to the cava, porta vein, and SMVs.
Infrequent injury to the major abdominal veins is largely due to the protection provided by surrounding organs and the retroperitoneum. Penetrating trauma accounts for 95% of injury to these structures. Stab wounds yield a slightly better survival than injuries produced by gunshot wounds or blunt injuries. The American Association for the Surgery of Trauma includes injuries to the major abdominal veins in the Organ Injury Scale for Abdominal Vascular Trauma ( Table 12-1 ). Not surprisingly, the most common cause of death is exsanguination, whether in the field or intraoperatively.
| Grade | Description |
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| Grade 1 |
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| Grade 2 |
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| Grade 3 |
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| Grade 4 |
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| Grade 5 |
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* This classification system is applicable to extraparenchymal vascular injuries. If the vessel injury is within 2 cm of the organ parenchyma, refer to the specific organ injury scale. Increase one grade for multiple grade 3 or 4 injuries involving >50% vessel circumference. Downgrade one grade if <25% vessel circumference laceration for grades 4 or 5.
Patients with major venous injuries who survive to the hospital may present in profound shock or may be relatively stable. A recent report of patients sustaining these injuries documented an average hospital admission systolic blood pressure of 90 mm Hg and a heart rate of 95 beats per minute. In addition to lower blood pressure, nonsurvivors following abdominal venous trauma also had a higher injury severity score (ISS), had more associated injuries, were older, and had greater blood loss at laparotomy. Considering quantity of hemorrhage, a blood loss of greater than 7.2 L has been associated with mortality, while patients with major vein injuries require an average of 19 units of packed cells with 7 L of crystalloid. Some authors have also found Glasgow Coma Scale (GCS) to be a statistically significant predictor of mortality. This association may variably represent degree of shock or associated injuries.
Associated injuries are almost uniformly found in patients with trauma to the major abdominal veins, due to their intimate association with key visceral and vascular structures. Asensio et al documented two to four associated organ injuries for every visceral vessel damaged. Among intraabdominal organs, the liver and stomach tend to be most frequently injured with trauma to the IVC, PV, and SMV. Injuries to the liver may be especially challenging, as attempts to mobilize the organ can place torque on the associated vascular structures with worsening of the vascular rent. Injury to a major venous structure is also frequently accompanied by damage to the associated artery, including the hepatic arteries, the aorta, and the superior mesenteric artery. In a review of the subject by Coimbra, 94% of portal and superior mesenteric venous injuries had associated intraabdominal injuries, with 61% of these including other major vascular injuries (most commonly IVC and superior mesenteric artery [SMA]). With 35% of superior mesenteric arterial injuries having associated SMV injuries, close apposition of major structures places all at risk. Additional work from the same group demonstrated the impact of multiple vascular injuries on survival. From a cohort of 302 patients with injuries to the abdominal vasculature, those with a single injured vessel had a mortality rate of 45%. When two vessels were injured, the mortality rose to 60% and the mortality climbed to 73% if three vessels were injured. Injury to more than three intraabdominal vessels was uniformly fatal.
Complication rates are significant with such injuries. The genesis of postoperative complications is multifactorial and attributable to associated injuries, patient age, comorbidities, and degrees of shock and hemorrhage. General complications include respiratory failure, dehiscence, sepsis, and infection. Abdominal complications included thrombosis of the repaired vessel, abdominal compartment syndrome, unplanned return to the operating room (OR) for bleeding, a vasoactive medication requirement, and gastrointestinal complications. In survivors, late ischemia to either the gut or liver attributed to ligation of the vessel or prolonged occlusion during repair, are additional serious complications.
Preoperative Preparation
The most important components of preoperative preparation are entering the operating room with both thorough anatomic knowledge and with plans for vascular exposure, vascular control, and basic techniques for repair. Little other preoperative planning is possible in the hemodynamically unstable patient; the unstable patient must be taken directly to the operating room. However, not all patients with these injuries are in extremis. For some patients, preoperative imaging is limited to a positive focused assessment with sonography for trauma (FAST) exam. For others, the role of computed tomography (CT) will be defined by the nature of the injury. In penetrating abdominal trauma, CT will have a limited role that is relegated to its use in the stable patient who lacks peritoneal signs, and in whom the injury is thought to be extraperitoneal. CT is of benefit in the event of blunt injury to a major abdominal vein (primarily the IVC).
Identifying a caval injury on CT scan is challenging. Active extravasation of contrast from the IVC is not typically seen in the hemodynamically stable patient. The most common indication of an underlying major vein injury is a retroperitoneal hematoma. Approximately 75% to 91% of retroperitoneal hematomas develop in zone I, 18% of patients will demonstrate a zone II hematoma, and 9% will have a zone III hematoma. The presence of retroperitoneal blood should raise suspicion for a major abdominal vessel injury; zone of occurrence does not necessarily reflect the involved vessel, though hematomas localized around the ascending colon and duodenum are fairly specific for IVC injuries. The retroperitoneum is capable of containing a large blood volume, up to half of the total blood volume, and serves to tamponade the bleeding from the relatively low-pressure venous system.
Additional CT findings may also indicate potential venous injury. A flat IVC on CT is a good indicator of hypovolemia and potential IVC pathology. A flat IVC is defined as one with a maximal transverse-to-anteroposterior ratio of less than 4 : 1. The presence of a flat IVC in conjunction with other injuries predicted the need for therapeutic intervention in 84% of the cases in one study. The flattened IVC as an indicator of pending hemodynamic collapse may be a useful finding in the trauma bay, because this finding can be detected with ultrasound. Subtle CT findings, peculiar to IVC injury, may include an irregular contour to the cava or a filling defect within the caval lumen. In rare cases, a herniation of pericaval fat into the vessel lumen may also indicate a laceration of the IVC. Exploration of these hematomas may be injudicious as it allows inadvertent release of torrential hemorrhage, to the detriment of the patient. While mechanism of injury and patient status may necessitate operative exploration, fore-warning of the severity of the venous injury allows the surgeon to plan the best approach and allows anesthesia and the remainder of the operative team to prepare for significant blood loss.
Despite all attempts, patients may deteriorate too rapidly for either radiologic study or even rapid admission to the operating room. In these cases, a resuscitative thoracotomy has been advocated in either the emergency department (ED) or the operating room (OR) as a bridge until more definitive therapy is accomplished. Currently, this approach is believed to be more harmful than beneficial, because significant negative metabolic and physiologic sequelae attend the opening of the thoracic cavity. Indications for ED thoracotomy are extremely limited, due to the very poor survival rate. Patients in whom resuscitative thoracotomy may be considered are those with witnessed arrest in penetrating injury and arrest following arrival in the hospital for blunt-trauma patients. A review of resuscitative thoracotomies used in the setting of abdominal vascular injuries, mostly arterial, over 30 years continues to demonstrate limited, but occasional, survival. A current literature review demonstrates a 10.5% (4 of 38) survival rate in patients undergoing resuscitative thoracotomy in the setting of abdominal vascular injuries. Those presenting with penetrating abdominal trauma, unstable hemodynamics, and a distended abdomen may benefit from this type of resuscitation. The maneuver significantly limits or stops ongoing blood loss and allows exploration and identification of the injury in a field free of ongoing hemorrhage. While thoracic access allows a much easier approach to the aorta for cross-clamping than that presented by the supraceliac aorta, it must be balanced by the additional insult. The incision creates a significant heat sink, and distal ischemia imposes a finite time constraint. Balancing benefits and risks is the surgeon’s continuous challenge.
Operative Management
The Inferior Vena Cava
Of the three major abdominal veins discussed in this chapter, the IVC is the most frequently damaged and requires some of the most complex decision making. The overall incidence of IVC injury ranges from 0.5% to 5% of penetrating injuries and 0.6% to 1% of blunt trauma. Approximately 30% to 50% of patients will die before reaching the hospital, either from exsanguination or associated injuries. Of the patients who survive to the hospital, 20% to 57% will not survive to discharge, either dying intraoperatively from exsanguination or during the precarious immediate postoperative period.
Penetrating injury to the IVC is slightly more common (0.5% to 5%) than is a blunt mechanism of injury (0.6% to 1%). When blunt IVC injury does occur, it is the result of torque on the vessel from extensive tributaries and retroperitoneal fixation. The retrohepatic cava in particular is protected by the hepatic ligaments, the retroperitoneum, and the hepatic parenchyma. Significant force must be sustained to tear or to avulse this structure, resulting in catastrophic injury.
Of all of major abdominal venous injuries, trauma to the IVC, whether blunt or penetrating, is the most amenable to nonoperative management. Because the IVC is a low-pressure (3 cm to 5 cm H 2 O) retroperitoneal structure, bleeding is initially contained within the confines of the retroperitoneum, allowing for tamponade of the injury. Studies with swine have found nonoperative management of IVC lacerations to be an effective strategy at times. Patients presenting hemodynamically stable with contained vena cava hematomas are candidates for nonoperative management. When the peritoneum is torn, however, the tamponade can be released. In order to minimize the likelihood of releasing the tamponade effect, vigorous intravenous fluid resuscitation should be avoided. Large-volume resuscitation will substantially enlarge the vena cava, including the injured region, and will increase the venous pressure with resulting hemorrhage. Similarly, those patients with penetrating major vascular injuries are the group most likely to benefit from fluid restriction and hypotensive resuscitation, by avoiding the effect of hydrostatically forcing the clot off the injured area. Patients with the potential for major abdominal venous injuries should not have intravenous fluids administered through lower extremity access sites. Obvious signs of deterioration, including hemodynamic instability, peritonitis, and changes in lactate level or base deficit, indicate failure of the current course of management and the need for surgical exploration.
The anatomy of the IVC impacts surgical decision making and patient outcome. The distal IVC arises from the confluence of the common iliac veins. Traveling cephalad through the right retroperitoneum, the vena cava receives venous outflow from several tributaries including lumbar vein, the right gonadal vein, both renal veins, the right adrenal vein and the inferior phrenic veins. The vena cava then traverses cephalad, posterior to the liver parenchyma. In many cases, the liver completely engulfs the vena cava, making retrohepatic exposure more challenging. At or immediately below the diaphragmatic hiatus, the hepatic veins join the IVC, including multiple small branches entering the lateral retrohepatic cava from the liver. After traversing the diaphragm, the proximal IVC enters the pericardium and drains into the right atrium.
For operative considerations, the IVC is divided into four anatomic segments: the infrarenal IVC, the suprarenal IVC, the retrohepatic IVC, and the suprahepatic IVC ( Fig. 12-1 ). Injuries to the infrarenal IVC have the best survival due to the relative ease of access and tolerance to ligation, when necessary. The suprarenal IVC remains relatively accessible but is more intimately associated with structures such as the kidneys, the pancreatic head, and the portal structures. Suprarenal ligation is poorly tolerated. The retrohepatic IVC is approximately 7 cm long and is directly behind, or within, the liver parenchyma. Injury to this subsegment almost invariably includes damage to the liver parenchyma, allowing free bleeding from the vein into the peritoneum via the injury tract through the liver. Exposure is very difficult and survival is poor. Finally, the suprahepatic IVC includes the course of the vessel from the dome of the liver to the right atrium, including the hepatic veins and the transition across the diaphragm. Mortality from injuries in this region approaches 100% due to difficulty gaining proximal and distal control in this extremely high-flow region. Due to the large diameter of this vessel and the difficulty of surgical access, in those rare circumstances when the injury is identified preoperatively, percutaneous interventional techniques will likely provide better salvage than open approaches.
Exposure and Mobilization
Access to the IVC is dependent on the portion that is injured. Upon identification of a large retroperitoneal hematoma suspicious for caval injury regardless of which segment, the cava is approached from the right. Specifically, the White Line of Toldt is divided along its length; and the ascending colon, hepatic flexure, and transverse colon are mobilized and reflected cephalad and to the patient’s left side or midline. An extensive Kocher maneuver is then performed, mobilizing the duodenum and pancreatic head leftward as well, using visualization of the left renal vein as the cue that mobilization is adequate ( Fig. 12-2 ) . Often, these maneuvers will expose a hematoma overlying the area of injury. In these cases, the hematoma should not be explored until a cogent operative plan is made. Although proximal and distal control of the IVC is advisable in most cases, this is not always possible. Even in instances where proximal and distal control can be achieved, significant bleeding may still occur from lumbar veins and other tributaries. Regardless of whether or not one has been able to accomplish proximal and distal control of the vena cava, if active hemorrhage is encountered, direct pressure on the area of injury should be applied. Then control may be achieved by starting proximal and distal to this region and “marching” toward the defect. In this manner, the site of injury may be localized without intermittent episodes of profuse bleeding. A common mistake is not dissecting down to the actual substance of the IVC and attempting to sew the peritoneal tissues in an effort to achieve hemostasis. Division of the overlying filmy tissues leads to identification of the substance of the IVC and a superior repair.
Control of the retrohepatic and suprahepatic portions of the IVC is particularly difficult to achieve given their friable nature and their anatomic location. Retraction of the liver upward will allow access to the most proximal portion of the infrahepatic IVC. Complete mobilization of the liver by division of the suspensory ligaments, including the right triangular, the coronary, and the falciform ligaments, will provide some mobility to access the retrohepatic portion of the cava. Attempts to mobilize the liver in this region, however, usually result in increased bleeding from the retrohepatic wound, as torque on the liver and IVC may increase the size of the laceration. Though lobar resection may seem appropriate, especially in cases of damaged liver parenchyma, this maneuver is generally discouraged. Removal of the overlying liver also removes the possibility of tamponade by the organ and adds disrupted liver parenchyma to sources of ongoing hemorrhage. Approach to the suprahepatic IVC will almost invariably require division of the diaphragm for adequate exposure. Additionally, a sternotomy may be indicated for proximal control of injuries to the suprahepatic IVC, as the infradiaphragmatic section of the IVC is not amenable to easy clamping and repair. Extreme care must be taken when working in this region to avoid dislodging thrombus from the injury or to disrupt the thin-walled hepatic veins from the cava. Percutaneous approaches that involve use of compliant endovascular balloons for inflow and outflow occlusion may be sought to address injuries to this portion of the IVC.
Control of Hemorrhage
If massive hemorrhage is encountered on entering the abdomen, immediate cross-clamping of the aorta is usually required. The standard vascular principle of proximal and distal control always applies, regardless of size and location of the vessel injury. Initial manual compression of the IVC allows visualization of the field of injury, in order to begin dissection. The traditional teaching is to apply sponge sticks above and below the wound for proximal and distal control. This technique can be problematic if not accomplished with great care, as forceful application may widen the injury, may create an iatrogenic injury, or may avulse a branch. Direct pressure on the area of injury is generally better starting with one’s fingers, which provides a gentler tactile application of pressure.
Although effective at controlling initial hemorrhage, this maneuver obscures the operative field and does not allow for use of that hand in exposing or repairing the injury. As such, the subsequent steps involve using other atraumatic, blunt instruments to maintain the control achieved with manual pressure. These instruments are often sponge sticks, which can then be replaced by lower-profile Kittner dissectors. In these instances, either the sponge stick or the Kittner dissector can be gently placed directly on or above and below the source of venous bleeding for control. The objective in this setting is to work back from the use of one’s fingers or hand to a visible and workable operative space to allow clearer dissection, visualization, and repair of the injury. The initial use of one’s hand, the sponge stick, or the Kittner dissector avoids having to place a larger metallic vascular clamp before the vena cava or the edges of the injury have been clearly defined.
The importance of good lighting, well-set and wide retraction, and multiple suction devices cannot be overemphasized in accomplishing these steps. In the case of linear injuries to the major abdominal veins, the vein edges may be grasped with Judd-Allis clamps and closed either with a Satinsky clamp or sutures ( Fig. 12-3 ). A simple stitch placed at the proximal and distal extent of the laceration, with accompanying gentle upward traction, will also elevate and collapse the laceration. This allows control of hemorrhage and exposure for primary suture closure. Another consideration in repair of the IVC and other large vein injuries is use of a larger noncutting needle (e.g., 4-0 polypropylene on an small half [SH] needle) that can be visualized and directed in the presence of considerable amounts of blood. Although well intended, too small a needle often becomes submerged in blood and is not able to be directed with intention; therefore it is prone to extending the original injury. Another common misstep is not dissecting down to the actual substance of the IVC wall and attempting to blindly place a clamp or to sew the peritoneal tissues in an attempt to achieve hemostasis. Division of the overlying filmy tissues leads to identification of the substance of the wall of the IVC and allows for control and suture repair of the injury.
Hemorrhage control presents unique challenges in the case of blunt retrohepatic and suprahepatic IVC injuries. The IVC injury is usually combined with significant hepatic parenchymal disruption. Hemorrhage results from both the disrupted liver parenchyma and from the retroperitoneum. Visualization and identification of the precise area of injury is particularly difficult. In this circumstance, direct pressure consists of compressing the liver parenchyma to reapproximate tissues and directing pressure posteriorly until anesthesia is able to catch up with blood loss. A Pringle maneuver should be utilized if the liver parenchyma is contributing to the hemorrhage. Complete mobilization of the liver, including division of the triangular and coronary ligaments and retroperitoneal attachments, should be carefully weighed in the circumstance of retrohepatic caval injuries. When hematoma is identified behind the hepatic suspensory ligaments, division of the ligaments should be avoided. With the liver completely mobile, existing tamponade is released and it will not be possible to reestablish tamponade with a freely floating liver. Control by direct pressure may be difficult and incomplete, and adjunctive endovascular techniques may be beneficial. The use of a compliant percutaneous endovascular occlusion balloon may provide a superior option for control of hemorrhage. Inflation of the balloons can provide a bloodless field, allowing time to obtain traditional proximal and distal control with vessel loops or even to allow immediate primary repair. If circumstances permit, occlusive balloons should be introduced and positioned via percutaneous access before exposing the injury to keep the site free for repair. The proximal and distal balloons may be introduced via bilateral femoral vein sticks or via a combined femoral and internal jugular approach. In some cases, insertion through the site of injury may be more expeditious. Endovascular grafts are also options for hemorrhage control in the patient with multiple injuries. In these cases, an endovascular graft may be inserted to cover the injury site and to allow control of the bleeding while other injuries are addressed.
Total hepatic vascular exclusion may be employed to control hemorrhage with profound bleeding from the perihepatic IVC or the liver parenchyma. This requires control of the suprahepatic and infrahepatic IVC. Because there is little room between the diaphragm and the liver to place a clamp or vessel loop for suprahepatic control, this maneuver requires either sternotomy or right thoracoabdominal incision with division of the diaphragm. A Pringle maneuver completes the isolation. In theory, bleeding should be controlled with total hepatic exclusion. In actuality, these maneuvers only decrease hemorrhage by approximately 40% to 60%. While these maneuvers slow bleeding, repair needs to be expeditious. Warm ischemia must be limited to 45 to 60 minutes. Intermittent release of the Pringle clamp should be performed. Unfortunately, this results in resumption of bleeding. Broering et al have proposed changing the nature of the ischemia to a cold-ischemia protocol. By infusing the liver with cold preservation solution, ischemia time may be prolonged, allowing better opportunity for repair. However, in these exceedingly unstable, hypothermic patients such complex procedures are rarely successful.
If hepatic isolation is inadequate to allow visualization and repair, total abdominal vascular exclusion is required. In addition to occlusion of the IVC and the performance of a Pringle maneuver, a supraceliac aortic clamp is placed to prevent all inflow to abdominal and distal structures. The loss of venous return in an already-hypotensive patient often leads to full arrest. While mortality is very high, an occasional patient in this extreme state will survive.
Considerations for Venous Repair
Following hemorrhage control and injury identification, attention is directed to the details of vascular repair. As with any elective procedure, standard principles of vascular surgery are applied. These principles include adequate proximal and distal control, not just to control bleeding but to provide enough vessel length to work. Ligation and division of branch vessels often provide mobilization and enhanced injury exposure. Primary repair is the preferred method of management. The vascular injury should be irrigated with heparinized saline to remove clots and allow adequate inspection of the vessel. If the edges of the injured site are jagged and their viability compromised, débridement is required to ensure the integrity of the suture line, but débridement should be judicious in order to minimize narrowing and subsequent thrombosis. Closing longitudinal tears transversely will minimize narrowing; that is not possible with long tears. Repairs are done with fine monofilament suture. Bites should be adequate to avoid the suture tearing through the tissue, but attention is paid to avoidance of excessive tissue incorporation in order to minimize narrowing. One should consider using a larger needle with the fine monofilament suture to allow visualization and direction in significant amounts of blood.
Application of the technique of primary repair for the venous injury will depend on the location of the injury, the extent of vein disrupted, and the associated injuries. When primary repair is not possible, end-to-end anastomosis, patch angioplasty, graft interposition, and ligation should be considerations. The most important factor in the decision for repair versus ligation is the patient’s physiologic status. Because all options beyond primary repair take significant time to complete, critically unstable patients who are cold, coagulopathic, and acidotic are not candidates. In those instances, the choice is usually limited to damage control measures with ligation.
Ligation
Ligation of the infrarenal IVC, iliac veins and left renal vein are tolerated fairly well. Conversely, ligation of the portal vein and the SMV are poorly tolerated; and ligation of the right renal vein often results in loss of the kidney. As expected, ligation is more successful when an abundant collateral circulation exists.
Caval ligation is well described in the literature. It is associated with a high mortality, primarily due to the instability of those patients requiring a damage control approach. Experience in multiple wars of the 20th century resulted in ligation standing as an accepted practice to address injuries to the cava. Ligation remains a relatively common practice in dealing with caval injuries in the modern era. Navsaria et al practiced ligation in 63% of patients cared for in one series. Huerta et al ligated one third of 36 caval injuries for a survival rate of 41.7%. Sullivan et al reviewed 100 IVC injuries collected over a 13-year time period. Of patients with infrarenal IVC injuries, 43% underwent ligation. As a group, patients undergoing ligation had a 41% early mortality rate and a 59% overall mortality rate. While patients in the repair group fared better with an early and overall mortality rate of 21%, the patients in the ligation group were significantly more ill. Suprarenal caval ligation is even more poorly tolerated with a high mortality rate, unless the patient happens to have existing generous collaterals with the azygos and lumbar venous systems. Ligation of the vena cava at or above the retrohepatic segment is uniformly fatal.
Hesitation to ligate the major abdominal veins stems not only from mortality concerns but from the potential sequelae of ligation. A major consideration following ligation of the infrarenal IVC is swelling of the lower extremities, potentially severe enough to cause acute compartment syndrome. Some groups advocate for prophylactic fasciotomy in patients undergoing ligation of the vena cava. In a recent publication on the topic by Sullivan et al, prophylactic fasciotomy was performed in three quarters of patients who underwent ligation of the IVC, as opposed to 4% of patients who underwent IVC repair. Follow-up of nine patients with IVC ligation in this series from Grady Memorial Hospital demonstrated that none had more than trace residual lower extremity edema in follow-up. Another series of 30 IVC ligations noted some lower extremity edema but found no need to proceed to fasciotomy in any patient. Earlier studies by Lucas and Ledgerwood of infrarenal IVC ligation further support the supposition that, if the patient survives the initial insult, few long-term sequelae result from the ligation of this vessel. Therefore, fasciotomy is not recommended as a routine prophylactic measure following IVC ligation. Rather, as part of the patient’s postoperative care, close monitoring of the compartments of the lower extremities should be routine. A low index of suspicion should result in rapid fasciotomy should there be evidence of rising compartment pressures.
Reconstructive Techniques
When hemodynamic and physiologic stability are ensured, more complex repairs of the vena cava can be considered. Though some narrowing may be expected and accepted following venorrhaphy, attempts to primarily close injuries that are greater than 50% circumference of the cava may result in excessive restriction of luminal size, subsequent thrombus formation, and even complete thrombosis. The method of repair largely depends on extent of venous injury. The combination of an anterior and posterior caval laceration is common. In the infrarenal portion of the cava, adequate mobilization may allow visualization of the posterior aspect of the vessel with direct repair by gentle rotation of the vena cava. When possible, knots should be kept extraluminal to remove a nidus of thrombus formation. More proximally, rotation of the vessel is usually not possible due to the tethering effect of the renal veins and the liver. In these situations, the anterior venotomy can be extended to allow repair of the posterior rent from inside the vessel lumen (see Fig. 12-3 ). Knots will necessarily be intraluminal for the posterior repair. Transected vessels may be amenable to an end-to-end anastomosis, although it is rare that such a patient would be stable enough to tolerate more than ligation. End-to-end anastomosis is more difficult in the vena cava compared to an extremity vein. Due to the tethering of the visceral and lumbar tributaries, mobilization of the vena cava to increase length is difficult. This is especially true where segments of the vessel have been lost to traumatic mechanism or where débridement is required. If loss of length prevents an end-to-end anastomosis, interposition grafting is a consideration.
The large caliber of the cava is such that standard saphenous vein interposition will not provide adequate luminal size, though saphenous vein may be used to construct a spiral vein graft (see Fig. 12-4 ). The internal jugular or external iliac veins are large-caliber donor options that may be used for caval interposition. A significant amount of time is required for vessel acquisition and reconstruction with these techniques, and this must be considered when deciding whether the patient is stable for such repair.
The Portal Vein
Injury to the portal vein is uncommon, documented in one series at 0.1% of all traumatic injuries over 20 years. Morbidity and mortality associated with portal vein injury is high. There is also a high frequency of major associated injuries, especially in the region of the portal triad. In a multiinstitutional review of 99 portal triad injuries, survival was only 20% if more than one portal structure was damaged. Of patients with portal triad injuries who died in the operating room, 85% had at least a portal vein injury.
The portal vein is formed from the confluence of the splenic vein and the SMV behind the neck of the pancreas ( Fig. 12-5 ). Contained within the hepatoduodenal ligament, the closely associated hepatic artery and bile ducts are frequently injured at the same time. The average diameter of the portal vein is 2 cm. Despite a high flow rate, approaching 1 L/min, pressures are low at approximately 10 mm Hg or less.
Exposure and Mobilization
The portal vein is best approached from the right. The ascending colon and hepatic flexure are reflected to the midline or the patient’s left. A wide Kocher maneuver, with leftward reflection of the duodenum and pancreatic head allows near complete exposure of the portal vein and associated structures. The common bile duct may be isolated and retracted leftward as well to provide additional access to the anterior surface of the vein. Division of the pancreatic neck may be necessary to access more distal portions of the portal vein. A Pringle maneuver (an atraumatic clamp, vessel loop, umbilical tape, or manual pressure is used to occlude the portal structures) is often needed to control hemorrhage while the portal structures are being mobilized.
Control of Hemorrhage
In the circumstance of massive hemorrhage, proximal control will consist of supraceliac aortic control. This may be the only way to reasonably control the inflow—both splenic flow from the celiac axis and superior mesenteric flow. In less-dire circumstances, the Pringle maneuver is generally the most useful method of controlling hemorrhage from suprapancreatic portal vein injuries. However, this makes dissection and exposure of the injury area quite difficult. Even in more limited injuries, the occlusive tape or clamp prevents visualization of the injury site. Indiscriminate clamping should be avoided to prevent injury to delicate structures in the region. Local proximal and distal control is obtained with the assistance of direct compression while dissecting the vein free from the hepatic artery and bile duct. Here again, working back from the effective application of manual pressure with one’s fingers or hand can be accomplished with gentle application of small sponge sticks or lower-profile Kittner dissecting sponges. Once the injury is visualized, it can be gently grasped with Judd-Allis clamps and mobilized to allow suture closure or passage of vascular tapes.
Repair of Portal Venous Injuries
Repair of the portal vein follows the general principles outlined for the vena cava. After the venous edges have been débrided to healthy tissue, the surgeon must decide if a primary repair is possible. Simple repairs should be performed using 5-0 or 6-0 monofilament suture in an interrupted fashion. If the portal vein has been divided, an end-to-end anastomosis may be accomplished if there is minimal tension between the two ends. Behind the pancreas, small medial tributaries entering the portal vein may be ligated and divided to achieve additional length. Additionally, if it has not already been done to achieve control, partial division of the pancreas and ligation of small medial tributaries may provide satisfactory mobilization to make anastomosis possible. Reverse saphenous vein interposition grafting is feasible, but few patients are stable enough to permit this approach. In cases in which repair is not feasible, the only alternative is ligation.
Portal Vein Ligation
As previously noted, patients with portal venous injuries usually sustain massive blood loss, have multiple associated injuries, and present in a state of extremis, which is not tolerant of prolonged repair. From a review of 18 patients presenting to the hospital with portal venous injuries between 1958 and 1980, survival was limited to 13% when ligation was used as a last-ditch salvage option. However, when the portal vein was ligated before cardiovascular collapse, survival improved to 80%. Survival following portal vein ligation is variably reported as 10% to 85%. Portal ligation is less well tolerated than caval ligation. If portal vein ligation is required, the anesthesia team must be made aware. Up to 50% of the blood volume may be sequestered in the splanchnic circulation. Ligation results in decreased venous return with subsequent splanchnic hypertension but systemic hypoperfusion. Aggressive fluid administration, both intraoperatively and in the ICU, are required. Patients develop massive visceral swelling due to the portal venous congestion.
The reported high mortality rates likely are partially related to failure of appreciation of the tremendous fluid requirements. However, many reports of high mortality following portal vein ligation were made before our appreciation of abdominal compartment syndrome and the benefits of temporary abdominal closure. Contemporary fluid and wound management will likely improve outcomes with portal vein ligation.
Delayed complications are common. Low mesenteric flow combined with shock may lead to venous thrombosis, bowel ischemia, and necrosis. The degree of bowel infarction may vary from patchy necrosis to near total small bowel infarction. Additionally, portal vein thrombosis and portal hypertension may occur as sequelae in this setting. The complications of portal vein ligation are sobering but are unavoidable when ligation is the only option to control hemorrhage and to provide immediate patient survival.
The Superior Mesenteric Vein
The SMV is infrequently injured and is reported to account for 0.1% of traumatic injuries. These injuries are most commonly produced by penetrating mechanisms. When injuries result from blunt mechanisms, damage occurs due to shear forces exerted on the mobile mesentery, resulting in avulsion of the vessel. Due to its close association with the SMA, the vessels are often injured in tandem. Found to the right of the SMA, the vein provides outflow for the jejunum, the ileum, the appendix, and the colon to the midtransverse segment. Portions of the pancreas and duodenum are also dependent on the SMV for outflow.
Due to the central location of the SMV, associated injuries are common. In a study focusing on 51 patients with SMV injuries, the average number of co-injuries was 3.5. As with all the major abdominal veins, mortality is high with reported rates varying between 50% and 71%, depending on the number of associated vascular and solid organ injuries.
Exposure and Mobilization
While relatively more accessible than the portal vein, the proximal portions of the SMV may require division of the pancreas for successful access. Anatomically intimate to the SMA and the other major visceral and vascular structures, exposure is further complicated when associated injuries are present in the region.
The SMV is quite accessible in its distal portion compared to the other major abdominal veins and is approached operatively in the same manner as the SMA ( Fig. 12-6 ). A direct approach at the base of the mesentery may be appropriate if injury occurs several centimeters below the inferior border of the pancreas. Medial visceral rotation may be necessary to access the root of the mesentery. If very proximal SMV control is required, then exposure mirrors that used for the portal vein. Colon mobilization and a Kocher maneuver are used to provide access, and the body of the pancreas must be divided to gain proximal control.
Hemorrhage Control and Repair
Distal SMV injury may be controlled with manual occlusion. Subsequent dissection will permit placement of tapes and clamps for proximal and distal occlusion. A proximal SMV injury will require pancreatic division to access, as noted above. Hemorrhage is copious with proximal SMV injury, and poor exposure can lead to visually impaired suture ligation, resulting in compromised hemostasis and iatrogenic injury to neighboring structures. Hemorrhage may be temporarily lessened by occlusion of the distal SMV and a Pringle maneuver, though back-bleeding from the splenic vein may still complicate the field to some extent. These maneuvers may be adequate to slow hemorrhage and to allow adequate mobilization of the proximal SMV. Primary repair of the SMV may be accomplished with interrupted 5-0 or 6-0 monofilament suture. In cases where significant tissue loss precludes primary repair, a saphenous vein interposition graft may be required.
Ligation of the Superior Mesenteric Vein
Surgical literature suggests that patients with SMV ligation fare better than those requiring portal vein ligation. Various studies describe a 15% to 33% mortality for SMV ligation, as opposed to a 36% to 43% mortality in the repair group. Asensio et al found no difference in mortality in 84 patients, 53 of whom underwent SMV ligation. Overall, these reports indicate that patients requiring ligation of the SMV will likely tolerate the procedure and may fare as well as those having venous repair. The possibility of splanchnic hypertension and late bowel ischemia exist with SMV ligation, as they do with ligation of the portal vein. Those patients surviving SMV ligation should undergo second look to evaluate viability of the intestines before definitive abdominal closure. Whether it is for the SMV, the portal vein, or the IVC, ligation should not be left to a last-ditch option, by which time the patient has crossed into irrecoverable shock. Judgment and composure are required to recognize the need for ligation and to accomplish it quickly before loss of massive quantities of blood in futile attempts at repair.
Temporary shunts should be considered for portal and superior mesenteric venous injuries in a subset of unstable patients whose injury anatomy is such that a shunt can be inserted without causing further damage. The relative low flow in the venous system in comparison to the arterial system will result in a higher rate of thrombosis of those shunts. However, this may provide additional options; and, if thrombosis occurs, the end result would be no different than with ligation.
The Inferior Vena Cava
Of the three major abdominal veins discussed in this chapter, the IVC is the most frequently damaged and requires some of the most complex decision making. The overall incidence of IVC injury ranges from 0.5% to 5% of penetrating injuries and 0.6% to 1% of blunt trauma. Approximately 30% to 50% of patients will die before reaching the hospital, either from exsanguination or associated injuries. Of the patients who survive to the hospital, 20% to 57% will not survive to discharge, either dying intraoperatively from exsanguination or during the precarious immediate postoperative period.
Penetrating injury to the IVC is slightly more common (0.5% to 5%) than is a blunt mechanism of injury (0.6% to 1%). When blunt IVC injury does occur, it is the result of torque on the vessel from extensive tributaries and retroperitoneal fixation. The retrohepatic cava in particular is protected by the hepatic ligaments, the retroperitoneum, and the hepatic parenchyma. Significant force must be sustained to tear or to avulse this structure, resulting in catastrophic injury.
Of all of major abdominal venous injuries, trauma to the IVC, whether blunt or penetrating, is the most amenable to nonoperative management. Because the IVC is a low-pressure (3 cm to 5 cm H 2 O) retroperitoneal structure, bleeding is initially contained within the confines of the retroperitoneum, allowing for tamponade of the injury. Studies with swine have found nonoperative management of IVC lacerations to be an effective strategy at times. Patients presenting hemodynamically stable with contained vena cava hematomas are candidates for nonoperative management. When the peritoneum is torn, however, the tamponade can be released. In order to minimize the likelihood of releasing the tamponade effect, vigorous intravenous fluid resuscitation should be avoided. Large-volume resuscitation will substantially enlarge the vena cava, including the injured region, and will increase the venous pressure with resulting hemorrhage. Similarly, those patients with penetrating major vascular injuries are the group most likely to benefit from fluid restriction and hypotensive resuscitation, by avoiding the effect of hydrostatically forcing the clot off the injured area. Patients with the potential for major abdominal venous injuries should not have intravenous fluids administered through lower extremity access sites. Obvious signs of deterioration, including hemodynamic instability, peritonitis, and changes in lactate level or base deficit, indicate failure of the current course of management and the need for surgical exploration.
The anatomy of the IVC impacts surgical decision making and patient outcome. The distal IVC arises from the confluence of the common iliac veins. Traveling cephalad through the right retroperitoneum, the vena cava receives venous outflow from several tributaries including lumbar vein, the right gonadal vein, both renal veins, the right adrenal vein and the inferior phrenic veins. The vena cava then traverses cephalad, posterior to the liver parenchyma. In many cases, the liver completely engulfs the vena cava, making retrohepatic exposure more challenging. At or immediately below the diaphragmatic hiatus, the hepatic veins join the IVC, including multiple small branches entering the lateral retrohepatic cava from the liver. After traversing the diaphragm, the proximal IVC enters the pericardium and drains into the right atrium.
For operative considerations, the IVC is divided into four anatomic segments: the infrarenal IVC, the suprarenal IVC, the retrohepatic IVC, and the suprahepatic IVC ( Fig. 12-1 ). Injuries to the infrarenal IVC have the best survival due to the relative ease of access and tolerance to ligation, when necessary. The suprarenal IVC remains relatively accessible but is more intimately associated with structures such as the kidneys, the pancreatic head, and the portal structures. Suprarenal ligation is poorly tolerated. The retrohepatic IVC is approximately 7 cm long and is directly behind, or within, the liver parenchyma. Injury to this subsegment almost invariably includes damage to the liver parenchyma, allowing free bleeding from the vein into the peritoneum via the injury tract through the liver. Exposure is very difficult and survival is poor. Finally, the suprahepatic IVC includes the course of the vessel from the dome of the liver to the right atrium, including the hepatic veins and the transition across the diaphragm. Mortality from injuries in this region approaches 100% due to difficulty gaining proximal and distal control in this extremely high-flow region. Due to the large diameter of this vessel and the difficulty of surgical access, in those rare circumstances when the injury is identified preoperatively, percutaneous interventional techniques will likely provide better salvage than open approaches.
