Gastric erosion of the LAGB is a rare but serious complication of lap band placement . Rates of erosion vary according to case study, but most series report a rate between 0.5 and 1 % [5]. Erosion can present either early or late, depending on the cause. Early erosions, covered in another chapter, generally occur secondary to undetected intraoperative gastric trauma/injury. Late erosions occur slowly and chronically. The band penetrates the gastric lumen slowly enough that there is adequate time for a protective peritoneal layer to form over the band and attached tubing. Micro-erosions eventually give way to larger erosions, and the leaking gastric contents will track along the gastric band tubing to the port site. Finally, a clinically obvious port-site infection will emerge that will not respond to drainage and antibiotics. At this point, gastric erosion must be suspected.

Erosions must also be a consideration in patients with abdominal pain and chronic NSAID use, as gastric ulcers can be a predisposing factor to erosion formation. Loss of weight restriction despite band adjustments is also a common presentation of band erosion. Lastly, patients who have undergone prior band revision or who have had bands placed secondary to other bariatric procedures are more prone to erosion, and as such one should have a higher index of suspicion in this group.

As mentioned above, the presentation of gastric erosion is variable. The most common presenting symptom is port-site abscess, followed in descending order by port-site sinus, subphrenic abscess, unexplained weight gain, left pyelonephritis, band deflation, peritonitis, and mucus collection at the port site [6]. Definitive diagnosis is provided by upper GI endoscopy. As erosion is normally secondary to pressure ischemia from the band, most erosions occur anteriorly where the gastric fundus has been plicated over the band. Endoscopy should be visualized by sutures or band material, though small erosions can be difficult to detect.

Once the diagnosis of band erosion is established, treatment is removal of the offending band. This can usually be managed laparoscopically, though it may require lysis of dense adhesions between the omentum and abdominal wall, as well as adhesions to the left lobe of the liver. Dissection and identification of band tubing are essential in this process. The tubing can be followed to the buckle of the band, which can then be transected and easily removed. The gastric plication should not be taken down during the procedure. Once the gastric perforation is identified, it should be closed in two layers, if possible, and a drain may be left at the closure site. Furthermore, methylene blue testing through an orogastric tube may be performed to assess for any further leakage or missed gastrotomies. OR EGD may also be used to distend the stomach and check for a leak. Patients will then typically have an upper GI series performed on postoperative day 1, and can usually be discharged with oral antibiotics and a clear liquid diet. If there is a >50 % erosion of the band into the lumen, it can be removed endoscopically with a cutting wire. The particular wire that cuts the band is not FDA approved for use in the USA for this purpose. However outside the USA, the use of this technique for band removal has been described in the literature. The technique of using the wire is to remove the port surgically and divide the band tubing distal to the port. The cutting wire is placed endoscopically and cut the band and the band is extricated through the mouth. The patient gets an esophagram the following day [7].

Megaesophagus is a rare complication of gastric band placement . The gastric band can impair esophageal peristalsis and cause impaired relaxation of the lower esophageal sphincter. Over time, this can lead to esophageal dilation, termed megaesophagus. Symptoms include dysphagia, regurgitation of salivary contents, and severe acid reflux. Upper GI series demonstrates a dilated esophagus, and esophageal manometry shows either aperistalsis or secondary/tertiary peristaltic contractions . Arias et al. found the incidence of megaesophagus in gastric band patients to be approximately 2 % [8].

Initial treatment includes prompt deflation of the lap band. If symptoms and esophageal dilation do not improve after deflation, removal of the lap band system is the ultimate therapy [9].

Port-related complications are reported to occur in 5–10 % of patients with lap bands. Some of the more simple issues involved tube breakage or leakage from the port site. These leaks can be caused by needle perforations during failed adjustment settings, or tubing fatigue from long-standing ports [10]. Medical staff who are not well versed in lap band management may also attempt to drain the band using a regular needle instead of a Huber needle, which could shorten the life span of the device.

Ports have also been known to dislodge from their sutures after placement. Ideally, the port will be affixed to abdominal fascia, preferably the anterior rectus sheath. In certain patients it may be very difficult to identify a fascial layer, and the port may inadvertently be sutured to subcutaneous fat. If that happens, it can subsequently rotate in a way that makes it inaccessible to the surgeon. A simple abdominal X-ray can confirm positioning, and if the port cannot be accessed it may need surgical revision.

As mentioned earlier in the chapter, port-site infections that occur late in the patient’s operative course are evidence of gastric erosion until proven otherwise. Port-site infections should be treated with systemic antibiotic therapy for 2–3 weeks. If the infection does not subside with this treatment, further studies must be performed to rule out gastric erosion. Even if erosion is not the precipitating cause, recurrent infections may require port removal and replacement after the infection is adequately treated.