The left lateral section of the liver is retracted ventrally in order to expose the gastrohepatic ligament and gastroesophageal (GE) junction (Fig. 6.1). Aggressive retraction can cause an iatrogenic liver injury, such as a liver laceration or a “sub-Glisson” capsular hematoma formation. Additionally, excessive and prolonged compression of the liver can contribute to hepatic arterial ischemia with the potential for delayed liver abscess formation and sepsis. Gentle utilization of a self-retaining retractor may minimize movement and chances of an iatrogenic livery injury. Attention to the amount of time the liver remains retracted is important, and re-positioning may be required in prolonged cases.

Variation of the “standard” hepatic arterial anatomy is the norm, and surgeons must be aware of clinically relevant deviations. Specifically important during antireflux procedures, approximately 8–18% of patients may have either an “accessory” or “replaced” left hepatic artery contained within the gastrohepatic ligament (Fig. 6.1) [7, 8]. This aberrant artery typically originates from the left gastric artery, but may arise directly from the celiac trunk or aorta [9]. During LARS, it is frequently encountered during division of the gastrohepatic ligament for initial right crural exposure. Care must be taken to seek out and identify any aberrant left hepatic artery in order to avoid inadvertent transection. As a general rule, any aberrant left hepatic arterial branches should be identified and preserved, unless causing critical obstruction for safe dissection and mobilization. If vessel ligation is required, appropriate hemostatic maneuvers must be utilized to avoid perioperative hemorrhage. Additionally, in patients with underlying liver disease (i.e. cirrhosis, hepatic compromise), ligation of an aberrant left hepatic artery may lead to significant hepatic ischemia and therefore preservation should be attempted. In otherwise healthy patients, ligation of an accessory artery may lead to temporary elevation of liver transaminases [8]; however, if ligation of a fully “replaced” left hepatic artery is necessary, the risk of a delayed ischemia liver abscess must be considered.

As dissection continues along the right crus with division of the phrenoesophageal membrane, the vagal nerves are at risk for injury (Fig. 6.2). The incidence of iatrogenic vagal nerve injury during fundoplication is reported to be as high as 20% [10]. The left vagus lies anteriorly on the esophagus and may run through the gastroesophageal “fat pad”. The right vagus is encountered along the posterior esophagus and may be injured when creating the retroesophageal/retrogastric window. Both nerves should be carefully identified and preserved to prevent postoperative pyloric dysfunction, delayed gastric emptying, and post-vagotomy diarrhea. Post-fundoplication diarrhea is common (18–33%) and may be due to vagal injury or accelerated gastric emptying from the fundoplication itself [11]. It is worth noting however, that while the nerves should always be respected, Pellegrini et al. have proposed vagotomy as an alternative method for esophageal lengthening, without significant adverse effects [12].

Routine division of the short gastric vessels during LARS is controversial. Studies have failed to demonstrate a significant decrease in long-term postoperative dysphagia and gas-bloat syndrome after ligation of short gastric vessels [13, 14]. However, many surgeons prefer to ligate these vessels to allow for more extensive mobilization of the gastric fundus, as well as improved exposure to the posterior gastric space, to aid in fundoplication creation. Dissection begins along the mid-portion of the greater curvature of the stomach at the level of the inferior pole of the spleen and extends superiorly. Some of the short gastric vessels may directly supply the upper pole of the spleen and division can lead to infarction of the tip of the spleen. This is usually without consequence and no further intervention is required. If the short gastric vessels are poorly visualized, tearing or incomplete ligation can lead to excessive bleeding. Careful tissue handling between the operating and assistant surgeon is necessary to expose the short gastric vessels. Before attempting ligation, the surgeon must be sure the vessel is completely encompassed in the tissue-sealing device. Additionally, minimal tension should be placed on this tissue when sealing to avoid tearing with incomplete hemostasis. Besides the formal, well-known short gastric vessels, there often are posterior gastric vessels that run dorsally (the so-called “pancreatogastric vessels”). The surgeon should make a conscious effort to identify these vessels, as they can be a source of troubling bleeding, and if not divided may limit the mobility of the gastric fundus (Fig. 6.3). If significant short gastric vessel bleeding occurs, conversion to an open operation may be required to achieve hemostasis, as this situation is, at times, difficult to manage laparoscopically. Additionally, traction on the capsule of spleen can cause a splenic laceration or subcapsular hematoma. The overall incidence of splenic injury appears to be less than 3% [15]. Careful tissue handling around the spleen is paramount to safe LARS.

Extensive gastric retraction during crural dissection or short gastric ligation can lead to a serosal injury and/or full-thickness perforation. It is best to grasp the epiphrenic fat pad or use a babcock clamp to retract the fundus. Injury is more likely in patients with a shortened esophagus or a large hiatal hernia with intrathoracic adhesions. In the setting of a large paraesophageal hernia, gastric injury can occur from an unwise attempt to reduce the hernia contents instead of focusing on dissection and retraction of the hernia sac itself. Limiting traction to the hernia sac will prevent undue retraction on the stomach and will ultimately result in reduction of all herniated organs. Additionally, if using an energy device to ligate the short gastric vessels, it is best to stay at least 2–3 mm away from the gastric wall to prevent thermal injury and delayed perforation. Intraoperative gastric perforation or serosal injury can almost always be repaired primarily.

Esophageal perforation is a rare but serious complication of antireflux surgery. The incidence of esophageal injury appears to be less than 1%; however, it may increase in the setting of reoperative procedures or surgical team inexperience [15–17]. Typically, esophageal injury occurs by one of two mechanisms. The first mechanism of injury occurs by iatrogenic esophageal myotomy with mucosal perforation. This tends to occur when normal tissue planes are obscured by either inflammatory or scar tissue (usually in reoperative procedures), or when bleeding and inappropriate technique obscure the anatomic landmarks. This can occur with manipulation of the esophagus or stomach at the earlier stages of dissection of the right/left crus or when developing the retroesophageal window. As such, we recommend constant gentle tension be applied by grasping the gastroesophageal fat pad and careful precise bloodless dissection. Additionally, utilizing a penrose drain around the distal esophagus to assist with retraction during retroesophageal dissection and cruroplasty can help minimize the risk of injury. The second mechanism of esophageal injury is iatrogenic perforation by placement of the esophageal bougie dilators/sizers. This will be discussed below. If a perforation is encountered intraoperatively, it can be repaired primarily with a one- or two-layered closure depending on surgeon preference and the integrity of the esophageal tissue. Key to a successful repair is the identification/exposure of the proximal and distal limits of the mucosal injury that needs to be approximated in its entirety without tension.