The Physiology and pathophysiology of laparoscopic adjustable gastric bands

The laparoscopic adjustable gastric band (LAGB) has rapidly emerged as one of the most powerful medical interventions available. Originally a physically restrictive operation, evolution of the technique has resulted in what is now hypothesised to be a satiety inducing procedure. There is limited understanding of associated physiological processes; including oesophageal motility, transit and gastric emptying. Intraluminal pressure effects of the LAGB have not been identified. Recently, a new spectrum of poorly defined intermediate term complications have arisen; presenting a major diagnostic and management challenge. The adjustability of the LAGB offers the ideal opportunity to tailor the procedure, optimising outcomes and avoiding complications. This thesis sought to address key areas of knowledge deficiency relating to the clinically relevant physiology and pathophysiology of the LAGB. High resolution manometry studies showed that in successful patients the LAGB produces an intraluminal pressure of 26.9±19.8 mm Hg, immediately beneath the oesophago-gastric junction. Adding saline to the LAGB increased intraluminal pressure in a linear fashion (21.2±8.7 mm Hg/ml), after a threshold volume was reached. Lower oesophageal sphincter (LOS) basal tone was attenuated (11.2±6.9 mm Hg), although deglutitive relaxation was normal. A mean of 4.5±2.9 oesophageal contractions were required to clear a semi-solid bolus across the LAGB. Trans LAGB flow only occurred during oesophageal peristaltic contractions; separated by reflux events that stimulated repeat peristalsis. The LOS serves a contractile function in LAGB patients, increasing intrabolus pressure in the isobaric region above the LAGB. Incorporation of assessment of LOS contractility, defined as the lower oesophageal contractile segment, improved the sensitivity of manometric diagnostic criteria. A semi-solid stress contrast swallow protocol and high resolution manometry identified luminal dilatations above the LAGB and focal impairments in oesophageal motility where no abnormality had been seen on liquid contrast swallow. Abnormalities were classified as: Transhiatal (oesophageal) enlargement (31%), gastric enlargement (40%), pan-oesophageal dilatation with aperistalsis (6%), deficient oesophageal motility (11%) and anatomically normal (12%). Gastric enlargements responded well to revisional LAGB surgery provided oesophageal motility was intact. Oesophageal enlargements or deficient motility were not responsive to treatment. Mild impairment of oesophageal peristalsis was not found to be clinically significant. A new technique allowed visualisation of the LAGB during scintigraphic studies. Semi-solid transit into the infraband stomach was delayed following LAGB (11 vs. 2, p=0.001). Meal retention above the LAGB was not observed. Removing saline from the LAGB normalised transit. Gastric emptying was not affected by LAGB. Twelve months following LAGB satiety increased after both a standard fast (3.7±2.3 vs.4.8±2.1, p=0.04) and a standard semi-solid meal (5.9 vs. 7.8±1.7, p=0.003). In a cross sectional study 323 of 408 patients responded (79%). Expected ranges for reflux: 8.7±9.8 (0=no reflux, 72=severe reflux), dysphagia: 19.9±8.7 (0=no dysphagia, 45=total dysphagia to water) and frequency of regurgitation (mean once per week) were established. Weight loss was the only predictor of patient reported satisfaction (r2=0.46, p=0.01). This thesis has described physiological processes associated with LAGB, the mechanisms of bolus transit and the intraluminal effects of adjustments. The LAGB was shown to delay transit and induce satiety, without physically restricting meal size. New, sensitive diagnostic tests combined anatomical change with assessments of oesophageal motility; allowing the spectrum of intermediate term complications and their response to treatment to be defined. The future challenge is to translate these data to improvements in outcomes and better understand the mechanism of weight loss.