The mesenteric branches of the abdominal aorta include the celiac artery, SMA, and IMA. The celiac artery arises from the proximal abdominal aorta above the transverse mesocolon. The vessel ranges from 1 to 1.5 cm in length in most adults before dividing into the hepatic, splenic, and gastric branches. It is surrounded by a dense plexus of nervous and lymphatic tissue [1, 2]. The hepatic artery passes to the right posteriorly and enters the hepatoduodenal ligament just superior to the pylorus to the left of the common bile duct. The splenic artery, the largest of the celiac branches, courses inferiorly and to the left, posterior to the pancreas in the upper portion of the gland. The splenic artery gives off several dorsal pancreatic branches as well as the left gastroepiploic artery before entering the lienorenal ligament and dividing into the terminal splenic branches at the hilum of the spleen. The splenic artery also gives rise to the short gastric branches throughout its course. The left gastric artery ascends cephalad and laterally to the left to enter the lesser curvature of the stomach.

The SMA arises from the anterior aorta in close proximity to the celiac artery in the supramesocolic region of zone I. The first portion of the SMA passes first under the neck of the pancreas crossing the splenic vein, then over the uncinate process and third portion of the duodenum to enter the small bowel mesentery. SMA injuries can be classified according to the schema created by Fullen et al. in 1972, or by the AAST-OIS (Tables 18.1 and 18.2) [24]. The Fullen classification divides the SMA into the trunk, proximal branches (between the inferior pancreaticoduodenal and middle colic), middle branches (those distal to the middle colic), and terminal or segmental branches such as the jejuna and ileal arcades.

The IMA arises from the inframesocolic infrarenal abdominal aorta and travels in close proximity to the aorta as it courses caudad to emerge in the left lateral aspect of the colonic mesentery. Within the colonic mesentery, it gives off the left colic, sigmoidal, and superior rectal branches.

The portal venous system is created by the confluence of the SMV and splenic veins behind the neck of the pancreas at the level of the second lumbar vertebra. The IMV anatomy varies, but in general it will drain into either the splenic vein or less commonly into the SMV prior to their confluence. The portal vein forms at the superior aspect of the pancreas and enters the hepatoduodenal ligament where it travels posterior and lateral to the hepatic artery and common bile duct before entering the parenchyma of the liver in the hilum. The portal vein branches into left and right portal veins, the right then subsequently divides into superior and inferior branches.

The IVC courses along the right paravertebral portion of the retroperitoneum, and injuries are classified by location, as infrarenal, suprarenal, or retrohepatic/suprahepatic. The suprahepatic and retrohepatic IVC extend from the diaphragmatic hiatus through the liver. The suprarenal IVC extends from just below the inferior liver edge to the level of the renal vein insertion sites. The infrarenal IVC is defined by the portion of the IVC below the renal veins inferiorly to the bifurcation into the common iliac veins. A previous retrospective review of IVC injuries stratified by location showed no significant difference in mortality between suprarenal and infrarenal IVC injuries if retrohepatic IVC injuries were excluded [12]. Due to massive hemorrhage and a difficult operative approach, injuries to the retrohepatic and suprahepatic IVC carry the highest mortality rates even in experienced trauma centers [8, 9, 12, 23, 25, 26].

Exposure of the celiac artery is best approached via left medial visceral rotation [1, 2, 7]. In order to obtain proximal control of the supraceliac aorta proximal to the celiac root, it may be necessary to divide the median arcuate ligament and crura of the diaphragm. This exposure allows visualization of the left lateral and anterior aspect of the upper abdominal aorta as well as the roots of the celiac and SMA origins. Alternatively, exposure of the celiac root can be performed through the gastrohepatic ligament. This requires division of the left triangular ligament and mobilization of the left lobe of the liver to the right and the esophagus to the left. Once the injury is exposed and proximal and distal control obtained, the surgical options include ligation or repair. The celiac artery can be ligated safely if the SMA is patent due to extensive collateral circulation. In a series by Asensio, among 13 patients, 11 underwent ligation and 1 underwent primary repair, of the patients who underwent ligation 4 survived. The single patient who underwent primary repair in this series also survived. Graham reported on 13 patients with celiac injury of which 4 patients underwent ligation with a survival rate of 50 % [14]. Asensio and his group found no survivors among their extensive literature search who underwent complex repair, reanastomosis, or reimplantation [13]. There are no reports of significant bowel ischemia following celiac ligation; however, ischemia and necrosis of the gallbladder after ligation is described, and cholecystectomy is advocated in all patients [2, 13]. Injury to branches of the celiac artery is also rare. The gastric and gastroduodenal branches can generally be ligated with little ill effects due to the extensive collateral flow from other celiac branches, as well as from SMA branches.

Hepatic artery ligation is generally well tolerated owing to the dual blood supply of the liver in conjunction with the portal vein and collateral flow from the gastroduodenal artery (GDA) if the ligation occurs distal to the GDA. When ligation occurs proximal to the GDA, decreased arterial blood flow to the liver may cause transient increase in liver transaminases, as opposed to elevations seen solely with parenchymal liver damage; this ischemic hepatitis is also associated with elevations in lactate dehydrogenase. Compromised arterial flow can also lead to biliary strictures as the arterial flow provides the primary blood supply to the ductal epithelium. Although rare, this can result in biliary strictures and cholangiectasis with resultant obstructive jaundice and occasionally cholangitis [31].

Splenic artery ligation just proximal to its terminal branch point is well tolerated if required for irreparable injury or uncontrollable bleeding. Although most often performed in conjunction with splenectomy as associated solid organ injury is common, the spleen if undamaged and not ischemic can be left in situ following ligation of the splenic artery. Most studies of splenic artery ligation for trauma have occurred in children where splenic salvage is common following both blunt and penetrating trauma. These studies demonstrate that in the majority of patients the spleen is viable following ligation and has normal immunological function [32, 33]. One study of splenic artery ligation without splenectomy in adult trauma patients had similar outcomes with no deaths and no need for reoperation following ligation [33].

Surgical approach to the SMA varies somewhat according to the location of injury. Injuries to Fullen zone I are best approached via a left medial visceral rotation [2]. Fullen zone II injuries are approached via visceral rotation, but transection of the neck of the pancreas may be necessary to visualize the injury and gain distal vascular control. Injuries in this location may also be approached by opening the root of the mesentery beneath the pancreas via the lesser sac [3]. Fullen zone III injuries are approached by dividing the ligament of Treitz to expose the suprarenal aorta and distal SMA trunk. They can also be exposed by performing an extended Kocher maneuver, mobilizing the duodenal C-loop until the SMA is encountered as it comes out from beneath the neck of the pancreas. Fullen zone IV injuries are best approached directly through the mesentery. Once the injury is exposed, proximal and distal control should be obtained [1, 3, 6, 7].

In hemodynamically normal patients primary repair is utilized for injuries in all zones if possible, this can be accomplished in 22–40 % of cases [5, 15]. The edges of the injury are debrided to healthy tissue and re-approximated with monofilament nonabsorbable sutures. Large defects, however, are unlikely to come together primarily as branching of the SMA makes significant mobilization impossible. In these cases techniques such as vein patch, interposition graft, and reimplantation have all been described.

In hemodynamically abnormal patients rapid primary repair may be considered; however, if the defect is large or difficult to expose, it should be ligated or shunted. Historically, ligation of the SMA is reported to be well tolerated in the proximal trunk because of collateral flow through the celiac axis, while ligation of distal injuries was discouraged due to the risk of bowel ischemia [3]. However, in two large series by Asensio, the authors found ligation to be commonly used in distal injuries. Ligation of both proximal and distal injuries was tolerated, but mortality was higher when ligating proximal compared to distal injuries [5]. It should be kept in mind that bowel ischemia may result if multiple distal injuries are ligated.