Band Migration/Dysphagia

The incidence of band migration is significantly higher with an earlier technique of band placement that involves perigastric dissection and the direct placement of the band on the stomach wall. The incidence has been reduced with technique modification, which involves band placement through the pars flaccida without exposure of the stomach wall. Band migration is also associated with pre‐operative BMI. Patients with pre‐operative BMI < 40 kg m⁻² are more likely to experience band migration than do those with higher BMI.

Migration involves the displacement of part of the stomach through a migrated band ring, which is usually positioned at a 45° oblique angle below the gastro‐oesophageal junction. Cephalad band migration can lead to anterior stomach prolapse, creating an acute angle between the gastric pouch and the oesophagus. However, a caudally displaced band creates posterior gastric prolapse, leading to the formation of a new gastric pouch.

Dysphagia is one of the most widely known complications of post‐operative gastric banding migration, with an incidence rate of 1–3%. Other symptoms, such as abdominal pain and tachycardia, can result from ischemic changes to the herniated stomach pouch.

The multiple‐view barium swallow test is typically used for diagnosis; it can help identify a displaced band with the prolapsed stomach wall.

Approaches to managing band migration vary from least invasive methods, such as band deflation, to immediate surgical interventions. Deflation is usually sufficient in the presence of mild symptoms. However, immediate surgical intervention is necessary when signs indicating gastric ischemia arise, including persistent pain, tachycardia and elevated lactic acid level.

Band Erosion

Band erosion through the stomach wall usually progresses slowly over an extended period. On average, the process occurs two years after band placement. The incidence of erosion is estimated to reach 7% after gastric banding. The mechanism of erosion may be attributed to the ischemic changes to the gastric wall adjacent to the band area, caused by an excessively stagnant band, thermal injury during band placement or mechanical injury related to the band buckle.

Patients with this complication may present with nausea, vomiting, epigastric pain or failure to achieve adequate weight loss as the band loses its restrictive effect. They may also present with recurring infections at the access site/port caused by gastric bacterial flora migrating along the tubing system. Sinister complications, such as hematemesis, can also occur if the band erodes to the left gastric artery or its branches on the stomach posterior wall. Acute abdominal pain with peritonitis rarely occurs because band erosion usually progresses slowly.

Endoscopy has both diagnostic and therapeutic uses in band erosion. The eroded band may be removed endoscopically, particularly when the band buckle is visible. Alternatively, it may be removed laparoscopically. Different approaches have been described for the laparoscopic removal of an eroded gastric band. One technique includes anterior wall gastrotomy with the intragastric transection of the band and the subsequent delivery of the band. The site of erosion is usually surrounded by inflammatory tissue, and closing it is not always feasible. The anterior wall gastrotomy should be closed without dissecting the external perigastric inflammatory tissues at the eroded band site. The site of erosion usually closes itself; however, an external drain should be placed to control any effluent until the erosion heals. A second technique includes the dissection of the perigastric tissue surrounding the band with the release and delivery of the band. Exposing the external site of gastric wall erosion for proper repair is not always possible because of inflammatory changes in the surrounding tissue; this usually heals on its own, but a drain should be placed. A second bariatric procedure should not be conducted during the same surgical session after removing an eroded gastric band or it would lead to a leak. Instead, the procedure should be deferred for three months to allow the local inflammation to subside and the stomach to heal. Subsequently, reassessment by upper endoscopy should be conducted before performing a revision surgery to minimise the risk of subsequent complications. In some cases of band erosion without significant signs of sepsis, band removal may be deferred for many months for complete intragastric migration to facilitate endoscopic removal.

Access Port Infection

On average, port infection has been reported in 0.3–9% of patients who have undergone gastric banding. This complication may be a primary infection associated with foreign body infection or secondary to band erosion. Port infection presents with local inflammatory symptoms, including erythema, pain, tenderness and possible fever if associated with an abscess collection. Elevated biochemical inflammatory markers and CT scan imaging can confirm the diagnosis. Upper endoscopy should be performed to rule out gastric wall erosion. The access port site is a foreign body; thus, an infection mandates removal by cleaning the subcutaneous pocket and secondary wound healing. However, removing the remaining band and tubing depends on patient presentation. The band and tubing may at times be salvaged by separating the port site, ligating the tubing and returning it to the peritoneal cavity with subsequent antibiotics, serial follow‐up of biochemical markers and possible repeat CT scan imaging. However, re‐infection may still occur. Thus, removing the gastric band and providing an alternative revisional procedure is a definitive approach. A simultaneous revision should be avoided if the infection clinically or radiologically involves the gastric band or if the gastric wall erosion is caused by the band.

Gastro‐Oesophageal Reflux

Gastric banding can also be associated with symptoms of significant reflux disease and oesophagitis. This can be attributed to stasis in a poorly functioning lower oesophagus, oesophageal dilatation or pseudoachalasia syndrome secondary to excessive back pressure created by a tight band or abnormal eating behaviour such as binge eating. These changes in the lower oesophagus can lead to the development of food intolerance, epigastric pain and reflux symptoms.

First‐line therapy in band‐related reflux disease or oesophageal dilatation is usually conservative, consisting of band deflation, administration of antacid medications, and diet intake behavioural modification. If these measures fail, band removal is indicated. Conversion to other bariatric procedures such as SG or RYGB can also be performed with band removal surgery for the purpose of maintaining weight loss.

Stricture

Stricture formation is an expected complication of SG, reported at 3.5% in some series. Acute cases are mainly caused by tissue oedema or kinking, whereas chronic conditions primarily arise from surgical factors. The proposed aetiology of chronic stricture formation mainly includes (i) over‐traction on the greater curvature while stapling particularly in the area across the incisura angularis or proximally close to the hiatus; (ii) axial deviation of the stapler line caused by inadequate dissection, creating a functional twist and (iii) use of a smaller bougie (usually smaller than 36 French). The two most common sites of stenosis are the gastroesophageal junction and incisura angularis. The presenting symptoms can vary depending on the degree of stenosis; it may include oral food intolerance, dysphagia, nausea and vomiting.

A work‐up tool for diagnosing stenosis can include endoscopy and CT imaging. Under more challenging conditions, such as the presence of a functional twist, a UGI contrast study can help determine the area of possible stenosis when the results of using other investigating tools are usually equivocal. In such cases, real‐time imaging is conducted while the patient is asked to ingest oatmeal mixed with contrast material.

Treatment approaches usually vary depending on the timing of presentation. In acute cases (which are mainly due to post‐operative tissue oedema), conservative treatment is usually sufficient until the oedema resolves spontaneously and completely. Treatment alternatives for persistent stenosis usually start with endoscopic balloon dilatation, particularly in a smaller stricture segment. The reported success rate attributed to endoscopic dilation is up to 56% in some case series. Placing a self‐expanding stent for managing strictures can present different challenges, such as poor tolerance and stent migration. Surgery is normally reserved for long‐segment stenosis or when symptoms fail to resolve after multiple attempts at endoscopic dilatation. These methods may include anterior wall stricture gastroplasty, followed by an omental patch. Another surgical alternative is conversion to RYGB or wedge resection with gastro–gastrostomy. Conversion to RYGB may also be used as a first‐line treatment for functional strictures caused by an acute axial deviation in the stapler line.

Reflux Disease

Gastroesophageal reflux is amongst the list of complications that may be encountered post‐SG. It presents with classical reflux symptoms, such as epigastric pain, heartburn and regurgitation. It can be caused by either the worsening of pre‐existing reflux (which is why severe GERD is a relative contraindication to SG) or the development of de novo reflux symptoms. Reflux can be attributed to either possible anatomical change encountered post‐SG, such as weakness of the lower oesophageal sphincter. It can also be secondary to mechanical causes, such as overly dilated fundus (‘sandglass’ deformity), distal stenosis due to mid‐corporal stricture or kinking and hiatal hernia left behind without repair. Work‐up for post‐SG reflux includes endoscopy, CT and upper GI contrast study.

A treatment plan needs to be tailored based on the underlying causes. In general, starting with the anti‐reflux medication is advocated in the absence of any mechanical causes.

For reflux cases secondary to strictures, endoscopic stricture dilation may be considered first before any further surgical intervention. Conversion to RYGB is the mainstay of treatment in cases refractory to medical treatment or in the presence of underlying mechanical causes as it is associated with a high rate of symptom control.

Leak

A staple line leak is a dreadful post‐SG surgical complication. The incidence of SG leaks ranges from 2 to 3%. Leaks are classified as either acute (<5 days post‐operatively) or chronic (>4 weeks post‐operatively) and are usually confined to the upper third of the sleeve. The aetiology is multifactorial – it can be due to tissue ischemic changes (tissue injury by energy devices or disruption of end arteries arising from the left gastric artery during overzealous dissection of the posterior wall of the stomach in the proximal fundus) or can be secondary to mechanical causes such as distal stenosis, a large fundus remnant due to inadequate dissection. Leaks can also occur if a relatively large stapler is used in an area close to the angle of His, where the stomach wall is thinner than the remaining part of the stomach. Some studies have reported that using a large staple height in this area may not be suitable for adequate tissue sealing.

The severity of SG is divided into two types: Type 1, which is characterised by a localised leak without generalised systematic manifestation, and Type II, which is characterised by diffuse leaks in the abdominal or pleural cavity. Incomplete healing of a leak may lead to the formation of a chronic fistula. Other causes include primary mechanical challenges, such as an increase in a relatively higher intraluminal pressure in the SG.

A chronic leak may vary in presentation. It can be asymptomatic or present with features of sepsis. It can also distinctly present with symptoms associated with a fistula to other systems (e.g. chest pain and productive cough in a fistula involving the lung).

Chronic leak management can be stratified into non‐surgical or surgical interventions.

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