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Abdominal Vascular Trauma

April 12, 2022 - read ≈ 18 min



Zach M. Feldman, MD MSc.

Division of Vascular and Endovascular Surgery, Massachusetts General Hospital, Boston, MA, USA


Jahan Mohebali, MD MPH.

Division of Vascular and Endovascular Surgery, Massachusetts General Hospital, Boston, MA, USA



Abdominal vascular injuries represent a grave threat to the victim of penetrating abdominal trauma, requiring expeditious diagnosis, judicious resuscitation and perioperative management, and swift surgical exposure and control. Early recognition and management of abdominal vascular injuries is paramount for improving patient survival.

Surgical Anatomy

The surgical anatomy of the abdomen is divided first into intraperitoneal and retroperitoneal compartments, and the retroperitoneum is further divided into four zones that influence management of abdominal vascular trauma.

  • Zone 1 comprises the midline retroperitoneum from the aortic hiatus of the diaphragm to the sacral promontory, including the aorta, inferior vena cava (IVC), and proximal visceral vessels.
  • Zone 2 is bilateral and consists of the kidneys, paracolic gutters, and distal renal vessels, in addition to the ureter and distal gonadal vessels.
  • Zone 3 includes the pelvic retroperitoneum from the mid-distal common iliac through external iliac vessels.
  • Zone 4 is often described as the perihepatic area, including the retrohepatic IVC and hepatic veins.

Clinical Presentation

The clinical presentation of abdominal vascular injury is highly dependent on the size and location of injured vessels, time since injury, mechanism of injury, and presence of concomitant injuries. Surgeons should maintain a high degree of suspicion for abdominal vascular injury, especially in the presence of hypotension and abdominal distention. However, transient normotension can be present, especially if bleeding is slowed via containment in the retroperitoneum or by adjacent tissues. Asymmetric femoral pulses may indicate unilateral iliac arterial injury, but beyond this, most diagnostic progress is made intraoperatively.

Significant intraabdominal hemorrhage, especially with violation of the peritoneum and communication between the retroperitoneal and free intraperitoneal spaces, can lead to abdominal compartment syndrome. On presentation, patients may have a tense abdomen, tachycardia, oliguria, and high plateau pressures with positive pressure ventilation. Similar characteristics may be present in postoperative patients with a closed abdomen, with additional perioperative risk factors including aortic cross-clamping, prolonged hypotension or hypothermia, and massive transfusion.

Diagnostic Evaluation

Although negative laparotomies should be minimized, the value of laparotomy in rapid diagnosis, exposure, and management of abdominal vascular injury cannot be overstated. The EAST Trauma Guidelines advise routine laparotomy in cases of penetrating abdominal injury with peritonitis, diffuse abdominal tenderness, or hemodynamic instability.[1]

In more resourced settings, diagnostic laparoscopy may be used in cases of penetrating abdominal injury with low suspicion of vascular injury, and computed tomography may be a useful diagnostic adjunct in stable patients for whom immediate laparotomy is not performed. If available, plain radiographs can assist in localizing bullet or shrapnel fragments.

In cases of blunt abdominal trauma, laparotomy is mandated by hemodynamic instability or peritonitis with a positive Focused Assessment with Sonography in Trauma (FAST) exam if ultrasound is available.


General Principles – Resuscitation and Nonsurgical Management

Prior to definitive surgical exposure and control, the use of resuscitation should be judicious. A principle of permissive hypotension should be followed, with a systolic blood pressure target of ~80-90mmHg.[2] Avoiding aggressive fluid resuscitation is paramount, as this increases rates and volume of hemorrhage and thus mortality.[3,4] However, resuscitation should be performed prior to massive exsanguination and hypotension that may precipitate cardiac arrest. Whole blood or blood products are preferred over crystalloid if available.

If available, resuscitative endovascular balloon occlusion of the aorta (REBOA) should be considered in cases of suspected abdominal vascular injury.[5] In this technique, percutaneous common femoral arterial access facilitates insertion of the occlusion balloon, which is inflated in the thoracic aorta, often without need of fluoroscopic guidance in emergent cases.

Endotracheal intubation should be avoided prior to arrival to the operating room or before full sterile prep in the case of abdominal vascular injury, as induction can often precipitate hemodynamic decompensation requiring immediate abdominal entry.[6]

General Principles – Surgical Management

Intraoperative management of abdominal vascular injury should prioritize a continuous and global reassessment of the patient at all times, with a focus on avoiding the triad of [1] hypothermia, [2] acidosis, and [3] hypocoagulability. Warmed fluids and warming blankets should be used if possible, and resuscitation should be with 1:1:1 ratio of red blood cells, plasma, and platelets when available.

Early aortic control should also be prioritized, with early laparotomy from xiphoid process to pubic symphysis facilitating aortic control either by direct compression or cross-clamping.

Retroperitoneal exploration of zone 1 hematomas is recommended, but exploration of stable non-expanding zone 2 or 3 hematomas may result in unsalvageable kidney injuries or uncontrollable pelvic bleeding.[6] All pulsatile, expanding, or leaking hematomas should be explored.

The intraoperative approach to retroperitoneal hematomas should consist of: hematoma opening, direct compression of active bleeding, bleeding vessel identification, and proximal and distal control.

After adequate control of the abdominal vascular injury, debridement of any devitalized tissue proceeds. This is followed by reconstruction. Ideal reconstruction of major arteries in the setting of trauma should proceed with autogenous conduit (frequently femoral vein or saphenous vein) given the risk of prosthetic graft contamination from intestinal injury or environmental sources.

If vein is not available, or vein harvest is likely to substantially prolong reconstruction in unstable patients, prosthetic grafts should be used with subsequent copious irrigation, omental or soft tissue coverage, and/or pre-emptive antibiotic soaking of the grafts to minimize the risk of infection. Typically, 3-0 polypropylene suture is used for the aorta, 4-0 to 5-0 for the iliac and femoral arteries, and 4-0 to 6-0 for visceral arteries and other branches.

General Principles – Damage Control Procedures

Damage control procedures should be considered early, prior to the development of irreversible shock, hypothermia, and coagulopathy. These procedures consist of liberal ligation of easily accessible venous injuries, packing of retroperitoneal or solid organ bleeding, and shunting of arterial injuries as opposed to definitive reconstruction.

Some arteries may be ligated in rare and extreme cases (e.g., the celiac axis, the inferior mesenteric artery), however the iliac arteries, superior mesenteric artery, and portal structures cannot typically be ligated without significant risk to life or limb.

Packing should be performed with sterile gauze, procoagulant-impregnated gauze, or sterile towels, with clear documentation of retained packing material for later retrieval. Shunting may proceed with Argyle or Sundt shunts; however if these are unavailable, temporary shunts may be made from sterile IV tubing, nasogastric tubing, or chest tubes depending on vessel size. Temporary abdominal closure is then performed using a vacuum dressing and the focus is then turned to continued resuscitation, rewarming, and correction of acidosis and coagulopathy prior to re-exploration and definitive vascular reconstruction, ideally within 24 hours.

Surgical Management – suprarenal aorta

Building upon the four-zone concept of the retroperitoneum, zone 1 injuries should be further divided into those that are supramesocolic/suprarenal, and those that are inframesocolic/infrarenal. This division occurs along an imaginary line at the level of the origin of the transverse mesocolon, pancreas, and duodenum. Because these structures sit across the aorta and are “fixed” in the retroperitoneum, adequate exposure generally requires specific maneuvers. Rapid proximal control, however, can be obtained before full exposure followed by necessary maneuvers.

To obtain rapid control, the left triangular ligament should be taken down with cautery and the left lobe of the liver mobilized with care taken to avoid tears to the hepatic veins. The stomach is pulled inferiorly and the pars flaccida of the gastro-hepatic ligament is opened to enter the lesser sac.

The GE junction and esophagus can be easily palpated at the crus of the diaphragm with the aid of a nasogastric tube. These structures are swept laterally so that the aortic pulse is easily palpated at the diaphragmatic hiatus. At this point, simple manual compression of the aorta against the spine or with an aortic compressor provides control. More definitive control can be achieved by dividing the crus of the diaphragm with cautery, identifying the aortic adventitia, bluntly spreading parallel to the aorta on either side, and placing a vascular clamp.

Circumferential control is generally not necessary and should be obtained with caution as avulsion of posterior intercostal branches can result in substantial hemorrhage that is exceedingly difficult to control in this location. If zone 1 hematomas extend cephalad and paradiaphragmatic control is necessary, the left crus of the diaphragm may be locally divided, a separate left thoracotomy may be made to enable thoracic aortic control, or the laparotomy may be extended into a thoracoabdominal incision.

Once control is obtained, a wider exposure of the proximal abdominal aorta is facilitated by a left medial visceral rotation to mobilize the foregut and pancreas, with or without bringing the left kidney off the great vessels in the retroperitoneal midline. The maneuver begins by taking down the left paracolic peritoneal reflection (the left white line of Toldt), sweeping the sigmoid and descending colons medially, and then continuing this maneuver up behind the splenic flexure, spleen, and tail of the pancreas.

Entering the Gerota’s fascia of the left kidney may facilitate elevating the kidney out of its bed to gain exposure to the infrarenal aorta as well. Identification and control of the left renal vein and artery should be obtained next. The left crus of the diaphragm can be taken down with cautery to achieve more proximal exposure. If the incision is extended into concomitant thoracotomy, division of the diaphragm will allow for exposure of the aorta from the arch to the bifurcation.

Surgical Management – infrarenal aorta

The infrarenal and in some cases suprarenal aorta may be approached from an inframesocolic exposure, although supraceliac control may be more prudent in the case of abdominal vascular injury without a priori knowledge of injury location. Inframesocolic exposure is approached via cephalad retraction of the transverse colon followed by release of the ligament of Treitz and mobilization of the duodenum and small bowel to the patient’s right. 

Surgical Management – visceral vessels

Injuries to the celiac axis should be exposed with a supramesocolic approach, either through the lesser sac or via medial visceral rotation. Especially in young patients without evidence of widespread vascular disease, the celiac artery can be ligated, as can the left gastric and splenic arteries. Common hepatic artery ligation can also be performed without concomitant portal venous or gastroduodenal artery injury.

Superior mesenteric artery (SMA) injuries should be managed based on the location of the suspected injury. Damage-control scenarios may permit SMA ligation, but only if distal to the middle colic artery, and may require bowel resection. SMA reconstruction should be performed if the injury is proximal to the middle colic artery, and may be shunted prior to definitive repair if necessary.

Concomitant pancreatic injuries mandate isolation of any vascular anastomoses from possible pancreatic enzyme leakage via omental or soft tissue wrapping and placement of suction drains. If available, on-table angiography can guide management of mesenteric root hematomas without obvious pulsatile bleeding or expansion, however empiric exploration is mandated in the case of ischemic bowel due to the likelihood of superior mesenteric artery (SMA) injury.

The retropancreatic SMA should be approached with left medial visceral rotation, but severe ongoing hemorrhage may require stapled pancreatic neck division for adequate exposure. Infrapancreatic SMA injuries may be approached via superior retraction of the pancreas, or by incision of the root of the mesentery with or without a Kocher maneuver.

Renal arterial injury management depends on timing and location of injury. As renal function is severely diminished after 3 hours of total ischemia or 6 hours of partial ischemia, reconstruction of renal arterial injuries should be performed within 6 hours of injury in most cases. After this point, particularly with severe concomitant injuries, nephrectomy may be preferable unless bilateral injuries have occurred or a solitary kidney is injured.

As a rule of thumb, approximately 1 in 3 patients will have accessory renal arteries. Renal artery injuries may be approached with right or left medial visceral rotation, and repair proceeds with arteriorrhaphy, vein patch, resection and re-anastomosis, interposition grafting, or autotransplantation to a remote site such as the external iliac artery. Extensive reconstructions should be accompanied by continuous cold perfusion of the affected kidney with University of Wisconsin solution if available,[7] or cold lactated Ringer’s solution. Renal vein injuries may be managed by lateral venorrhaphy or ligation.

Inferior mesenteric artery (IMA) injuries are rare, and IMA ligation can be performed with near impunity in young patients without evidence of widespread vascular disease.

Surgical Management – iliac vessels

Iliac vessel injury should be suspected with hypotension accompanying a penetrating injury in the lower abdomen or pelvis, pelvic fracture, or asymmetric femoral pulses. The common iliac arteries form at the aortic bifurcation typically at the L4-L5 level and divide into the external and internal iliac arteries at the level of the sacroiliac joint.

The iliac bifurcation frequently lies deep to the ureter. Iliac arterial or venous injury can result not only from penetrating injury, but in blunt or blast injuries with associated pelvic fracture, which can lead to vessel stretching over the site of bony abnormality. Concomitant iliac arterial and venous injuries are common, occurring in over 25% of cases.[8]

Iliac vessel exposure may be obtained via traditional laparotomy, but a narrow pelvis (particularly in males) may require an extension with a longitudinal incision through the inguinal ligament or transverse lower abdominal incision. Exposure should proceed with medial rotation of the right and left colon, and care should be taken to avoid injury to the ureter overlying the iliac bifurcation and iatrogenic injury to the iliac veins underlying the arteries.

In some cases, contained zone 3 venous injury (including intact posterior peritoneum) without expanding hematoma or hemodynamic instability may be observed as exploration in these situations is likely to result in substantial hemorrhage before control can be obtained. In some cases, it may be necessary to divide the right common iliac artery in order to fully expose the left common iliac vein for repair.

If torrential venous hemorrhage is encountered, pelvic packing may be of great utility. Substantial bilateral iliac vein compression is likely to initially worsen hemodynamic instability as a result of decreased venous return, which can be overcome with further volume resuscitation.

Lower extremity compartment syndrome is a significant risk in patients with severe iliac arterial injuries, or in cases where iliac venous injuries are treated with ligation. Fasciotomies should be performed based on the suspicion of the surgeon.

Surgical Management – inferior vena cava (IVC)

The IVC is the most commonly injured abdominal vessel, accounting for up to 25% of abdominal vascular injuries in one series.[9] Patients with isolated IVC injuries may be hemodynamically stable on presentation. Supramesocolic IVC injuries should be approached with similar intraoperative principles and early control of the proximal abdominal aorta.

However, in contrast to the aortic exposure, a right medial visceral rotation should be performed with hepatic flexure mobilization and the Kocher maneuver for duodenal mobilization. Exposure to the suprahepatic IVC or hepatic veins is often improved via extension to sternotomy or right thoracoabdominal incision.

Exposure of the retrohepatic IVC requires extensive mobilization of the liver with release of all ligaments and is typically assisted by a right subcostal or hockey stick incision. Packing should be attempted first in a damage-control scenario as this dissection is technically challenging and frequently results in large-volume blood loss with very high mortality. Often total hepatic vascular exclusion is required, consisting of infradiaphragmatic aortic cross-clamping followed by a Pringle maneuver (compression of the hepatoduodenal ligament), infrahepatic IVC clamping, and suprahepatic IVC clamping. Prior aortic cross-clamping is necessary for avoiding precipitous hypotension associated with the decreased venous return caused by IVC clamping.

Inframesocolic IVC injuries may be approached similarly to injuries of the inframesocolic aorta, with cephalad transverse colon retraction and rightward displacement of the small bowel.

IVC injuries may be repaired with lateral venorrhaphy in many cases, patch venoplasty, or interposition grafting. IVC ligation may be performed in extreme scenarios only if below the renal veins. IVC stenosis after repair, typically via lateral venorrhaphy, can precipitate thrombus formation and PE, so surgeons should maintain a low threshold for IVC filter placement postoperatively.

In extreme cases, the use of a an atrio-caval shunt may be helpful to control hemorrhage while maintaining venous return. This shunt typically consists of a chest or endotracheal tube placed through the right atrial appendage and down to the infrahepatic IVC. Cinching down on the cava around the tube forces returning lower extremity and renal blood into the tube where it is then carried and deposited to the right atrium. The tube is similarly cinched within the cava just above the diaphragm so as to isolate the retrohepatic IVC. When used with peri-hepatic packing, this temporizing maneuver may be life-saving until definitive exploration and repair can be performed.

Surgical Management – portal venous system

Injuries to the portal vein, superior mesenteric vein (SMV), and splenic vein can present with severe hypotension and typically require emergent exploration via laparotomy. Right colon mobilization and the Kocher maneuver facilitate exposure, however division of the neck of the pancreas with a vascular stapler should be considered if combined SMA and SMV injuries are present. Limited portal venous injuries may be repaired with lateral venorrhaphy and more complex venous injuries require definitive reconstruction with interposition grafting or patching, preferably autogenous saphenous vein. Portal vein ligation may be performed in extreme scenarios, with survival ranging from 55-85%,[10-13] but is not possible with concomitant hepatic artery injuries. These patients should be shunted prior to definitive reconstruction after resuscitation, as ligation of both hepatic artery and portal vein is not compatible with life.


  • Early recognition of abdominal vascular injuries is critical and should be guided by hypotension, abdominal tenderness or distention, and stigmata of thoracoabdominal or pelvic injury. Normotension may be present, especially in the case of some venous injuries or retroperitoneal tamponade
  • Aggressive resuscitation should be avoided initially, and permissive hypotension targeting systolic blood pressure of 80-90mmHg may improve hemorrhage control and survival
  • Early laparotomy facilitates rapid identification of injuries and should focus on immediate packing, hemorrhage control, proximal aortic control if necessary, and proximal and distal control of identified vascular injuries.
  • Damage-control procedures should be incorporated early if necessary, and consist of liberal venous ligation, shunting of arterial injuries, and temporary abdominal closure prior to definitive reconstruction.
  • Definitive reconstruction should proceed with autogenous graft when available.
  • Postoperative management should focus on aggressive correction of acidosis, hypothermia, and coagulopathy, with high suspicion for thrombosis or compromise of repaired vascular injuries


  1. Como JJ, Bokhari F, Chiu WC, Duane TM, Holevar MR, Tandoh MA, et al. Practice management guidelines for selective nonoperative management of penetrating abdominal trauma. The Journal of trauma [Internet]. 2010 Mar [cited 2022 Mar 21];68(3):721–33. Available from: https://pubmed-ncbi-nlm-nih-gov.treadwell.idm.oclc.org/20220426/
  2. Sondeen JL, Coppes VG, Holcomb JB. Blood pressure at which rebleeding occurs after resuscitation in swine with aortic injury. The Journal of trauma [Internet]. 2003 May 1 [cited 2022 Mar 16];54(5 Suppl). Available from: https://pubmed-ncbi-nlm-nih-gov.treadwell.idm.oclc.org/12768112/
  3. Stern SA, Dronen SC, Birrer P, Wang X. Effect of blood pressure on hemorrhage volume and survival in a near-fatal hemorrhage model incorporating a vascular injury. Annals of emergency medicine [Internet]. 1993 [cited 2022 Mar 16];22(2):155–63. Available from: https://pubmed-ncbi-nlm-nih-gov.treadwell.idm.oclc.org/8427424/
  4. Leppäniemi A, Soltero R, Burris D, Pikoulis E, Waasdorp C, Ratigan J, et al. Fluid resuscitation in a model of uncontrolled hemorrhage: too much too early, or too little too late? The Journal of surgical research [Internet]. 1996 Jul 1 [cited 2022 Mar 16];63(2):413–8. Available from: https://pubmed-ncbi-nlm-nih-gov.treadwell.idm.oclc.org/8661235/
  5. Stannard A, Eliason JL, Rasmussen TE. Resuscitative endovascular balloon occlusion of the aorta (REBOA) as an adjunct for hemorrhagic shock. The Journal of trauma [Internet]. 2011 Dec [cited 2022 Mar 16];71(6):1869–72. Available from: https://pubmed-ncbi-nlm-nih-gov.treadwell.idm.oclc.org/22182896/
  6. Demetriades D, Inaba K. Vascular Trauma: Abdominal. In: Sidawy A, Perler B, editors. Rutherford’s Vascular Surgery and Endovascular Therapy. 9th ed. Philadelphia, PA: Elsevier; 2019. p. 2391–409.
  7. Belzer FO, Southard JH. Organ preservation and transplantation. Progress in clinical and biological research. 1986;224:291–303.
  8. Demetriades D. Iliac Vessel Injuries. In: Rich N, editor. Vascular Trauma. Philadelphia, PA: WB Saunders; 2004. p. 339–51.
  9. Asensio JA, Chahwan S, Hanpeter D, Demetriades D, Forno W, Gambaro E, et al. Operative management and outcome of 302 abdominal vascular injuries. American journal of surgery [Internet]. 2000 [cited 2022 Mar 17];180(6):528–34. Available from: https://pubmed-ncbi-nlm-nih-gov.treadwell.idm.oclc.org/11182412/
  10. Stone HH, Fabian TC, Turkleson ML. Wounds of the portal venous system. World journal of surgery [Internet]. 1982 May [cited 2022 Mar 17];6(3):335–40. Available from: https://pubmed-ncbi-nlm-nih-gov.treadwell.idm.oclc.org/7113238/
  11. Mattox KL, Espada R, Beall AC. Traumatic injury to the portal vein. Annals of Surgery. 1975;181(5):519–22.
  12. Buckman J, Pathak AS, Badellino MM, Bradley KM. Portal vein injuries. Surgical Clinics of North America. 2001;81(6):1449–62.
  13. Petersen SR, Sheldon GF, Lim RC. Management of portal vein injuries. Journal of Trauma – Injury, Infection and Critical Care. 1979;19(8):616–20.
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