Inferior Vena Cava, Portal, and Mesenteric Venous Systems

Introduction

Injury to the large veins of the abdominal cavity, including the inferior vena cava (IVC) and the portal and the superior mesenteric veins is uncommon occurring in 5% of penetrating and 1% of blunt trauma cases. Because prehospital mortality associated with injury to these large veins ranges between 30% and 50%, there are relatively few patients who survive to have surgical repair. As such, even experienced trauma and vascular surgeons have a relatively limited practice with the operative management of these injury patterns. The literature has consistently reported mortality rates of 50% to 70% for injuries to the superior mesenteric vein (SMV), portal vein, and IVC. The mortality figures have been unchanging over several decades and thought to be refractory because of the difficulty in accessing the venous injury, both exposing and controlling, as well as the likelihood of torrential hemorrhage from these low-pressure, high-flow structures. The principles of operative exposure and repair that will be reviewed in this chapter have remained fairly consistent, though newly developed endovascular techniques offer promise in creating more effective approaches to certain of these highly lethal patterns of vascular trauma.

Historical references to abdominal venous injuries are limited mostly to case reports and oblique references in clinical series of combat injured. Some of the most comprehensive reviews among civilian patients have been published from the Baylor College of Medicine registry. 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 IMV injured in 0.4% of patients. An additional review of 4459 patients over 30 years found that 34% of the vascular injuries were to the abdominal vasculature and roughly 4% of these were to the mesenteric vessels.

As noted, the mortality associated with 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 specialized techniques have been published. The military’s experience using temporary vascular shunts has become a standard in civilian practice, providing a unique opportunity to control and temporize certain forms of venous injury while component-based resuscitation occurs. At the same time, resuscitative endovascular balloon occlusion of the aorta (REBOA) has become more common as an adjunct to quickly restore central aortic pressures (i.e., coronary and cerebral pressures) and stem bleeding in certain patterns of torso venous injury and shock. Aggressive options such as venovenous bypass and liver explantation are mostly anecdotal and uncommon, often impractical, methods to manage the bleeding patient.

The infrequent nature of abdominal venous injury is due to the relatively small size of the vessels and the fact that they are hidden or protected by the surrounding inferior costal margin, the viscera, and the retroperitoneum. Penetrating trauma accounts for 95% of injury to intraabdominal veins, with outcomes following stab wounds slightly better than those following injury from firearms or blunt mechanisms. The American Association for the Surgery of Trauma (AAST) includes injuries to the major abdominal veins in the Organ Injury Scale for Abdominal Vascular Trauma ( Table 19.1 ). Not surprisingly, the most common cause of death in these situations is exsanguination, whether in the prehospital setting or in the resuscitation or operating room.

Patients with major venous injuries who survive to the hospital often present in shock, although some will have reached a precarious state of equilibrium as the hypotension will have reduced the rate of bleeding. In situations in which permissive hypotension is effective, the patient may appear relatively stable. One report of patients sustaining these types of injuries documented an average hospital admission systolic blood pressure of 90 mm Hg and heart rate of 95 beats per minute. In addition to lower blood pressure, those who died also had higher overall injury severity (i.e., ISS), a greater number of associated injuries, were older, and had more blood loss at the time of laparotomy. A 7-liter blood loss has been shown as a threshold associated with higher mortality, while patients with major venous injuries require an average of 19 units of packed red blood cells and 7 liters of crystalloid. Given these daunting numbers, one should be in a damage control mindset when tackling this type of vascular trauma, looking for ways to expeditiously control or temporize bleeding while coordinating with the resuscitation team to maintain key elements of the patient’s overall physiology (e.g., temperature, acid/base status, coagulation profile, oxygenation).

Given the intimate anatomic proximity, patients with central venous trauma commonly have injuries to other intraabdominal structures such as viscera, solid organ, or ductal structures of the hepatobiliary or urogenital tracts. The liver and stomach are most commonly associated with intraabdominal venous trauma, although patients with injury to the vena cava or portal or superior mesenteric veins have, on average, between two and four additional injuries, including those to other large vessels. Concomitant liver injuries are especially challenging as attempts to mobilize the organ can place torque on the vena cava and/or portal vein and extend or worsen the primary venous injury. Injury to a major venous structure is frequently accompanied by damage to the adjacent artery, including the aorta and the hepatic and superior mesenteric arteries (SMA).

In a review by Coimbra, 94% of patients with portal and superior mesenteric venous trauma had associated intraabdominal injuries, with 61% of these being to other major blood vessels (most commonly the IVC and SMA). Just over one-third of SMA injuries (35%) have an associated injury to the of SMV. Additional findings from that clinical experience showed the impact of multiple vascular injuries on survival. From a cohort of 302 patients with abdominal vascular trauma, a single vessel injury had a mortality rate of 45%; when two vessels were injured, the mortality increased to 60%, and 73% when three vessels were injured. Injury to more than three intraabdominal vessels was uniformly fatal.

Complication rates are also high in the setting of intraabdominal venous trauma. The genesis of these is multifactorial, attributable to associated injuries, patient age and comorbidities, and severity of blood loss and shock. Common complications include but are not limited to pulmonary failure, renal failure, wound infection and dehiscence, and sepsis. Intraabdominal complications include thrombosis of the venous repair, abdominal compartment syndrome, reoperation for bleeding, a prolonged intensive care unit stay, including need for vasopressor support and gastrointestinal complications. In those who survive operative repair, delayed gut or liver ischemia resulting from vessel ligation or thrombosis (or just prolonged ischemia prior to the vessel repair) can result in postoperative complications and prolonged intensive care unit admissions.

Preoperative Preparation

The most important component of preoperative preparation is beginning the operation with a thorough understanding of anatomy and knowledge about how to expose and control the abdominal vascular injury. In many instances of central venous trauma, preoperative imaging is limited to only a focused assessment with sonography for trauma (FAST) examination as the unstable patient must be taken directly to the operating room. In these cases, it is often useful to enter the operation in a damage control mindset, looking for opportunities to expeditiously control bleeding and ways to restore flow, but also a willingness to ligate or shunt vessels and stage operations to optimize the patient’s resuscitation and physiological condition. In many instances a “second look” operation 12 to 24 hours after the first surgery is needed to assess for bleeding, viability of the viscera, and the need to perform definitive vascular repair.

Not all patients with intraabdominal venous trauma are hemodynamically unstable. The hematoma surrounding the injury may be contained within the retroperitoneum resulting in tamponade and a patient with normal vital signs or one who responds to small amounts of resuscitation. The utility of computed tomography (CT) depends on the nature and mechanism of injury. CT scan has less of a role in the immediate management of patients who have sustained penetrating abdominal trauma, especially those in who are hemodynamically normal or lacking peritoneal signs and in whom the penetrating injury is thought to be extraperitoneal. In contrast, CT is invaluable in the diagnosis and management of patients with significant blunt trauma, especially those with injury to a major abdominal vein such as the IVC. In the appropriate patient, detailed CT imaging allows the surgeon to gauge the need for an aggressive resuscitation and to develop a treatment plan that may range from nonoperative management, to a damage control operation, to the use of endovascular techniques.

Identifying an injury to the vena cava on CT may be challenging as contrast extravasation is often not seen, especially in the patient with relatively normal vital signs. The most common radiographic finding associated with a large vein injury is a retroperitoneal hematoma. Between 75% and 91% of retroperitoneal hematomas develop in zone I of the abdomen (i.e., central or midline), whereas 18% of patients will have a zone II hematoma (i.e., lateral spaces). Approximately 1 in 10 patients with abdominal venous injury will have radiographic evidence of a zone III or pelvic hematoma. The presence of retroperitoneal blood should raise suspicion for injury to a large abdominal vessel, remembering that the zone of the hematoma may not correspond anatomically to the injured vessel. One consistent anatomic association is that between a right lateral retroperitoneal hematoma (zone II) near the ascending colon and duodenum and an injury to the IVC. As noted previously, the retroperitoneum and surrounding visceral or solid organ structures often serve to contain and tamponade low-pressure venous bleeding.

Another CT finding that points to, or should raise suspicion regarding, a large venous injury is “flat” IVC which is an indicator of hypovolemia. A flat IVC is defined as having a maximal transverse-to-anteroposterior ratio of less than 4:1. The flat IVC can also be detected in the trauma bay using ultrasound and is a useful indicator of caval injury and/or pending hemodynamic collapse. Subtle findings, particularly in relation to IVC injury, include an irregular contour to the cava or a filling defect within the lumen on CT imaging. In rare cases, herniation of surrounding fat into the lumen of the vena cava may be present as an indication of vessel laceration. Nonoperative management (i.e., observation) of some retroperitoneal hematomas is indicated as open exposure of these injuries can release the tamponade and result in torrential hemorrhage.

The most hemodynamically depleted patients with abdominal venous trauma may deteriorate too rapidly for CT or ultrasound imaging or even transport to the operating room. In these cases, a resuscitative thoracotomy, either in the emergency department or in the operating room, should be considered as means to restore central aortic pressure and coronary and cerebral perfusion. This maneuver reduces or stops bleeding below the aortic clamp and maintains left ventricular afterload, preventing cardiac arrest until hemostasis can be obtained and the clamp slowly removed. Indications for thoracotomy are limited because of the low likelihood of survival in these scenarios. However, thoracotomy should be considered in patients who have penetrating trauma and a witnessed cardiac arrest (pre- or in-hospital), and in those having sustained blunt injury and who arrest after arrival to the hospital. One literature review on the topic showed a 10.5% (4 of 38) survival rate in patients undergoing resuscitative thoracotomy in the setting of abdominal vascular injury.

Although a left thoracotomy provides relatively easy access to the aorta for clamping, the exposure comes at a cost to the patient’s temperature, pulmonary function, and acid-base status, not to mention the morbidity of the incision itself. One alternative is a midline laparotomy with supraceliac clamping of the aorta at the diaphragmatic crus. This approach can be more anatomically constrained and difficult for those not familiar with the supraceliac exposure, but if performed quickly, it does accomplish the desired effects of resuscitative aortic occlusion and avoids opening the thoracic cavity.

REBOA is an appealing, less-invasive alternative to resuscitative thoracotomy for unstable patients or those progressing to a terminal degree of shock. Endovascular access to place the balloon catheter is achieved using a percutaneous or open femoral artery approach. In either instance, ultrasound can be used to identify the common femoral artery just below the inguinal ligament. The length of REBOA catheter to be inserted is estimated by placing the catheter on the outside of the patient and measuring the distance between the femoral artery and the desired aortic occlusion zone. For a suspected subdiaphragmatic, intraabdominal bleeding source, the balloon should be placed and inflated in aortic zone 1 which is between the origin of the left subclavian and the celiac arteries (i.e., supraceliac aorta). Zone III balloon positioning and inflation is indicated for patients with a pelvic bleeding source (e.g., severe pelvic fracture), and occurs between the renal arteries and the aortic bifurcation (i.e., infrarenal aorta).

Significantly less invasive than resuscitative thoracotomy, inflation of the REBOA balloon has the same hemodynamic and bleeding control effects as cross-clamping the aorta. REBOA limits or stops bleeding below or distal to the inflated balloon and increases central aortic pressure and perfusion to the coronary arteries and brain. Like other forms of external aortic cross-clamping, REBOA is only a temporizing maneuver that can be applied for 20 to 30 minutes until resuscitation can begin and efforts made at definitive hemorrhage control. Preclinical, large-animal studies have shown that REBOA is effective in decreasing blood loss, stabilizing central venous pressures, and improving survival in the setting of major venous injury.

Operative Management

The Inferior Vena Cava

Of the three major abdominal veins discussed in this chapter, the IVC is the most frequently injured and requires some of the most complex decision-making. The 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 with this injury pattern die prior to reaching the hospital, either from exsanguination or associated injuries. Of those who survive to the hospital, 20% to 57% will not survive to discharge, dying from bleeding in the operating room or during the early postoperative period.

Penetrating injury to the vena cava is slightly more common. However, the vena cava is relatively fixed in the retroperitoneum and in the setting of blunt trauma, there is torque and tearing of the vessel at one or more of the venous tributaries attached to the IVC. The retrohepatic cava is especially fixed in place, protected by the hepatic ligaments, the retroperitoneum, and the hepatic parenchyma. Significant force is required to tear or avulse the vena cava in this location, often resulting in a catastrophic injury.

Of all major abdominal veins, injury to the IVC, whether blunt or penetrating, is the most amenable to nonoperative management. As the IVC is a low-pressure (3–5 mm Hg) retroperitoneal structure, bleeding is initially contained within the confines of the retroperitoneum, allowing for tamponade of bleeding. Studies with swine have found that nonoperative management of IVC lacerations is effective in selective circumstances, especially instances in which the hematoma is contained and the patient’s hemodynamic status is stable. When the retroperitoneum is violated, the tamponade can be released into the peritoneal cavity resulting in much higher rates of bleeding and shock.

To minimize the likelihood of releasing the retroperitoneal tamponade, one should opt for permissive hypotension and avoid over resuscitation and arbitrarily increasing the patient’s blood pressure. Administering large volumes of resuscitation fluid (blood or crystalloid) will increase the venous pressure, enlarge the vena cava, including the injured segment, and increase the likelihood of bleeding. Similarly, patients with penetrating injuries are likely to benefit from fluid restriction and hypotensive resuscitation, a strategy which reduces the chances that hydrostatic pressure will force the clot off the tear in the vena cava. Patients in whom there is a suspicion for vena cava (or other major abdominal vein) injury, should not have resuscitation fluids administered through femoral venous or other lower extremity sites. Overt signs of deterioration, including worsening shock, peritonitis, and ominous changes in acid base status, indicate the need for surgical exploration.

The distal IVC arises from the confluence of the common iliac veins and as it courses cephalad through the right retroperitoneum, it receives venous flow from several tributaries including lumbar and the right gonadal veins, both renal veins, the right adrenal vein, and the inferior phrenic veins. More cephalad, the vena cava traverses posterior to the liver parenchyma (i.e., retrohepatic). 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 feed into the cava, including 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: infrarenal, suprarenal, retrohepatic, and suprahepatic ( Fig. 19.1 ). Injuries to the infrarenal IVC have the highest likelihood of 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 portal structures. Suprarenal ligation of the IVC is poorly tolerated. The retrohepatic IVC is approximately 7 cm in length and is directly behind, or within, the liver parenchyma. Injury to this segment 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 of the retrohepatic IVC is difficult, and survival from injuries in this location less likely. 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 high-flow region. Due to the large diameter of the IVC in this location and difficulty of surgical access, in the rare circumstances when this injury is identified preoperatively, percutaneous endovascular techniques will likely provide better salvage than open approaches.

Exposure and Mobilization

Access to the IVC depends on the anatomic segment that is injured. Upon identification of a retroperitoneal hematoma suspicious for caval injury, the vena cava should be approached from the patient’s right side. 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 to the patient’s left, using visualization of the left renal vein as the cue that mobilization is adequate ( Fig. 19.2 ). Often, these maneuvers will expose a hematoma overlying the area of injury. 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 occur from lumbar veins and other posterior tributaries. When hemorrhage is encountered, direct pressure on the area of injury should be applied. Control may then 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 in not dissecting down to the actual substance of the IVC and attempting to sew the peritoneal tissues that overlie the vena cava in a hurried effort to achieve hemostasis. Division of the overlying filmy retroperitoneal tissues will expose the actual wall of the IVC that needs to be seen to be débrided and repaired.

Control of the retrohepatic and suprahepatic portions of the IVC is particularly difficult to achieve given their friable nature and their anatomic location. Cephalad retraction of the liver 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, coronary, and falciform ligaments, will provide mobility to access the retrohepatic portion of the cava. However, attempts to mobilize the liver in this region often result in increased bleeding from the retrohepatic wound, as torque on the liver and IVC can increase the size of the laceration. Though lobar resection may seem appropriate, especially in cases of damaged liver parenchyma, this maneuver is discouraged and should be one of last resort. Removal of the overlying liver removes the possibility of tamponade by the organ and adds disrupted liver parenchyma as a source of bleeding. Endovascular approaches, including balloon occlusion of the IVC through remote femoral and/or jugular venous access, can offer a quick and safe alternative for temporary hemostasis to facilitate repair of caval injury in any of its anatomic segments.

Approach to the suprahepatic IVC will almost always require division of the diaphragm for exposure. Additionally, a sternotomy to access the intrapericardial IVC may be indicated for proximal control, as the infradiaphragmatic section of the IVC is not amenable to easy clamping and repair. Care must be taken when working in this region to avoid dislodging thrombus from the injury or disrupting the thin-walled hepatic veins inserting into the cava. As mentioned, percutaneous approaches that involve use of compliant endovascular balloons for inflow and outflow occlusion may be helpful in visualizing and repairing injuries to this portion of the IVC.

Bleeding Control

If massive hemorrhage is encountered at the time of laparotomy, temporary aortic occlusion may be required to support left ventricular afterload, avoid end stage shock, and prevent onset of a terminal cardiac rhythm. This can be accomplished by compressing or clamping the supraceliac aorta at the diaphragmatic hiatus or using REBOA inserted through one of the femoral arteries. The principles of proximal and distal control apply, regardless of size and location of the vessel injury. Initial manual compression of the IVC allows visualization of the field of injury, to begin dissection. The traditional teaching is to apply sponge sticks above and below the venous injury for proximal and distal control. This technique can be problematic if not accomplished with great care as forceful application may widen or create an iatrogenic injury or avulse a venous branch. Applying direct pressure with one’s fingers is often gentler and easier to control while localization of the injury is underway.

After localization of the injury, proximal and distal control with atraumatic blunt instruments should be achieved to free one’s hands for more detailed dissection of the vessel and eventual repair. Transitioning smaller, more focal instruments such as the low-profile Kittner dissectors (i.e., “peanut”) to compress proximal and distal to the injury is less likely to obscure or block key parts of the operative field from view. The smaller Kittner dissectors are a reasonable choice for control, as they can be gently placed directly on top of, or above and below, the source of bleeding. 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 dissectors avoids having to place larger metallic clamps in the field 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 overstated 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 with either a Satinsky clamp or 4-0 polypropylene sutures ( Fig. 19.3A ). 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 controls the bleeding and facilitates exposure for primary suture closure.

Another consideration when going to repair the IVC or other large venous injuries is to use a larger noncutting needle (e.g., 4-0 polypropylene on an SH needle). A larger needle is easier to visualize and direct in the presence of considerable amounts of blood. Although well-intended, too small of a needle is often submerged in blood and not able to be seen or appropriately guided which can prolong the repair and potentially extend the original injury. Another common misstep is in not dissecting down to the actual substance of vein wall and attempting to blindly place a clamp or to sew the overlying 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 and from the retroperitoneum. Visualization and identification of the exact area of injury is difficult. In this circumstance, direct pressure consists of compressing the liver parenchyma to reapproximate its anatomic form and pressuring posteriorly onto the injured and underlying vena cava as a means of tamponade until anesthesia can catch up with blood loss. A Pringle maneuver, in which a finger is introduced into the foramen of Winslow to encircle and occlude the structures of the porta hepatis, should be utilized if the liver parenchyma is contributing to the bleeding.

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 will not be possible to reestablish with a freely floating liver.

Control by direct pressure may be difficult or incomplete and adjunctive endovascular techniques may be beneficial in these circumstances. Specifically, the use of endovascular occlusion balloons may provide a better option for bleeding control. Inflation of the balloons proximal and distal to the injury site can provide a bloodless field, allowing time to obtain more direct proximal and distal control of the vessel with loops or clamps, or even allow immediate primary repair. If circumstances permit, occlusive balloons should be introduced and positioned via percutaneous access from above (i.e., transjugular) and below (i.e., transfemoral) prior to exposing the caval injury to lessen bleeding and keep the site free for repair. The balloon catheters may be introduced through both femoral veins, or using a combined femoral and internal jugular vein approach. In some cases, insertion and inflation of a balloon through the site of injury may be more expeditious. Endovascular stent grafts (i.e., covered stents) are also an option for hemorrhage control in the multiply injured patient. In these cases, the stent graft may be inserted to cover or seal the injury from within and control bleeding while other injuries are addressed.

In the setting of profound bleeding from the perihepatic IVC or liver parenchyma, total vascular exclusion may be necessary. This maneuver requires control of the supra- and infrahepatic IVC which may require a partial sternotomy or right thoracoabdominal incision to expose and clamp the limited length of vena cava between the diaphragmatic cruse and the liver itself. A Pringle maneuver to occlude portal vein and hepatic artery inflow completes vascular isolation and should stop all bleeding. In reality, total hepatic isolation may only stem the bleeding by 40% to 60%, but it should allow enough control to facilitate parenchymal or vascular injury repair. Because this series of operative steps induces warm ischemia, they can only be held for 45 to 60 minutes before inducing irreversible damage to the liver and hepatic failure. Intermittent release of the Pringle clamp to allow periods of perfusion should be performed if the occlusion time must be longer. Broering et al. have proposed extending a safe ischemic time period by infusing cold preservation solution with or without topical cooling of the liver. However, in these unstable, often hypothermic, patients such complex maneuvers are often not possible and 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 performance of a Pringle maneuver, a supraceliac aortic clamp or REBOA is placed to prevent all arterial inflow into the abdomen and distal structures. The loss of venous return in an already hypotensive patient often leads to full arrest. Although mortality is very high, an occasional patient in this extreme situation will survive.

Considerations for Venous Repair

After controlling the bleeding, attention is turned towards repairing the vessel. Thorough exposure, proximal and distal control, and careful dissection of enough vessel length on which to work are all important steps. Careful inspection for, and control of, branch vessels facilitates mobilization and prevents “back-bleeding” into the injured artery or vein. In most cases, prior to repair, the vessel should be opened with Potts scissors to inspect the backwall and intima and débride injured parts of the wall. The intima of the vessel should then be irrigated vigorously with heparinized saline to remove platelet aggregate and thrombus and allow further inspection of the lumen.

Primary repair is one method should the vessel have a sharp injury and maintained its length and diameter. If the edges of the injured site are jagged or their viability in question, they should be débrided with Potts scissors to ensure integrity of any subsequent suture line. Closing longitudinal tears transversely minimizes vessel narrowing. However, this maneuver is not advisable with long linear injuries which either need to be fixed with patch angioplasty or by placement of an interposition graft. Vessel repair is done with fine monofilament suture (4-0, 5-0, or 6-0 polypropylene) with enough purchase so that the suture does not pull through the wall. If primary repair is going to result in significant luminal narrowing, then one should consider using a synthetic or biologic patch angioplasty. As previously noted, in a bloody field, one should use a larger needle with the monofilament suture to be able to see and effectively maneuver.

The type of vascular reconstruction (primary repair versus patch angioplasty versus interposition graft) will depend on the location and extent of the venous injury and associated injuries. One should be mindful that in damage control scenarios, venous ligation may be the most appropriate approach. Although repairing the venous injury to maintain flow is appealing, any significant vascular reconstruction will take time, resources and more resuscitation. It is a difficult call to make, and one that should be made in conjunction with the anesthesia or resuscitation team, but in patients who are cold, coagulopathic, and acidotic, foregoing venous repair in favor of ligation may be the better part of valor.

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