“Surgery side effects are temporary. (bloating, flatulence and diarrhea – this can last a few weeks)”
“Eat a normal diet straight away – you can return to a normal diet”
“Some people experience symptoms similar to those caused by gallstones after surgery (tummy pain, indigestion, diarrhoea).”
“This is known as post-cholecystectomy syndrome (PCS) and it’s thought to be caused by bile leaking into areas such as the stomach or by gallstones being left in the bile ducts.”
“In most cases symptoms are mild and short-lived”
Source: Gallbladder Removal NHS
This is 100% False: The side effects listed are generally accessed as being lifelong. The human body digestive system is permanently disabled once the gallbladder is removed.
Post-cholecystectomy bile (duodenogastric) reflux.
Evidence based medical studies conclude bile reflux occurs in 20-30% of cholecystectomized persons. Those with Duodeno-gastric bile reflux are twice as likely to have had Cholecystectomy. Likely damage attributable to chronic bile exposure post-cholecystectomy includes:
- Cellular damage to esophagogastric junction
- Gastroesophageal Mucosal Injury ( mucosa is a membrane that lines various cavities in the body and covers the surface of internal organs)
- increase the incidence of gastric and esophageal cancer
- Barrett’s esophagus, 10% of patients with Barrett’s esophagus develop esophageal adenocarcinoma.
Evidence based medical studies source:
- Nudo R, Pasta V, Monti M, Vergine M, Picardi N. Correlation between post-cholecystectomy syndrome and biliary reflux gastritis. Endoscopic study. https://www.ncbi.nlm.nih.gov/pubmed/2699712
- Lorusso D1, Pezzolla F, Montesani C, Giorgio P, Caruso ML, Cavallini A, Guerra V, Misciagna G. Duodenogastric reflux and gastric histology after cholecystectomy with or without sphincteroplasty https://www.ncbi.nlm.nih.gov/pubmed/2253017
- Shah Gilani SN1, Bass GA1, Kharytaniuk N2, Downes MR3, Caffrey EF3, Tobbia I3, Walsh TN4. Gastroesophageal Mucosal Injury after Cholecystectomy: An Indication for Surveillance? https://doi.org/10.1016/j.jamcollsurg.2016.12.003
At Houston heartburn and Reflux Center, more than 50% of patients presenting for GERD evaluation have already underwent a cholecystectomy.
“Gastroesophageal Mucosal Injury after Cholecystectomy: An Indication for Surveillance?” is a new study published by T. Walsh et al in the current issue of JACS (Journal of the American College of Surgeons). The authors evaluate the incidence of stomach bile pooling detected by endoscopy in patients before and after cholecystectomy. They further measure the bile reflux index, cellular proliferation marker Ki67 and tumor-suppressor gene p53 in biopsies taken from the gastro-esophageal junction and gastric antrum. The analysis show that cholecystectomy increases the incidence of bile reflux and bile induced damage of gastric and esophageal mucosa. Chronic bile induced esophagitis and gastritis increase the incidence of gastric and esophageal cancer. The role of bile reflux in the pathogenesis of Barrett’s esophagus is well established and 10% of patients with Barrett’s esophagus develop esophageal adenocarcinoma.
Correlation between post-cholecystectomy syndrome and biliary reflux gastritis. Endoscopic study.
Experimental reports have proved that bile acids damage the gastric mucosa. Moreover it is now accepted that duodenogastric reflux occurs in 20-30% of cholecystectomized persons. The Authors, with the purpose of defining a correlation between gastric mucosa damage by duodeno-gastric reflux and postcholecystectomy syndrome have taken into consideration two groups of 14 patients each. To the first group belonged cholecystectomized patients, who had episodic, often postprandial pain, constant heart burn, with associated vomiting and Hypochromic anemia. To the second group belonged asymptomatic patients with previous cholecystectomy. All these patients were endoscoped (EGDS), and their endoscopic biopsy specimens were surveyed. 99Tc HIDA cholescintigraphy was performed in all the groups of patients, after endoscopy. In 85% of symptomatic patients we found, during endoscopy, reflux of bile into the stomach with associated reddish and inflammatory change of antral mucosa vs. 7.14% of the control group. Atrophic chronic gastritis was found in 71.43% of endoscopic biopsy specimens of Symptomatic vs. 14.28% of asymptomatic patients. Superficial chronic gastritis was found in 28.57% of symptomatic vs. 50% of asymptomatic patients. At last we found active atrophic or superficial antral gastritis (Whitehead) in 90% of symptomatic patients vs. 0% of asymptomatic people. The Authors conclude that there is a positive correlation between duodenogastric reflux and postcholecystectomy syndrome when biliary reflux is correlated with an histological finding of antral active chronic gastritis.
Br J Surg. 1990 Nov;77(11):1305-7.
Duodenogastric reflux and gastric histology after cholecystectomy with or without sphincteroplasty.Lorusso D1, Pezzolla F, Montesani C, Giorgio P, Caruso ML, Cavallini A, Guerra V, Misciagna G.
Sixteen patients who had undergone cholecystectomy plus sphincteroplasty, 14 cholecystectomized patients and ten control patients were studied to evaluate whether differences existed in duodenogastric reflux and whether these were related to morphological damage of the gastric mucosa. Duodenogastric bile reflux during fasting was evaluated by measuring the concentration of total bile acids (by an enzymatic method) and single bile acids in the gastric juice by high performance liquid chromatography. The damage was evaluated histologically by systematic endoscopic biopsy of the antrum and body of the stomach. There was a statistically significant difference in fasting bile reflux between the three groups (Kruskal-Wallis test, P less than 0.001), and the group that underwent cholecystectomy plus sphincteroplasty had a significantly higher median value than the cholecystectomized group (P less than 0.05) and the control group (P less than 0.01). The distribution of chronic antral atrophic and superficial gastritis was different in the three groups (chi 2 test, P less than 0.005). Chronic atrophic gastritis was associated with cholecystectomy plus sphincteroplasty (P less than 0.01), while chronic superficial gastritis was more frequent in cholecystectomized patients. These results suggest that there may be more duodenogastric reflux after cholecystectomy plus sphincteroplasty than after cholecystectomy alone, and that there may be a correlation between the amount of duodenogastric reflux and the severity of mucosal damage.J Am Coll Surg. 2017 Mar;224(3):319-326. doi: 10.1016/j.jamcollsurg.2016.12.003. Epub 2016 Dec 18.
Gastroesophageal Mucosal Injury after Cholecystectomy: An Indication for Surveillance?Shah Gilani SN1, Bass GA1, Kharytaniuk N2, Downes MR3, Caffrey EF3, Tobbia I3, Walsh TN4.
Cholecystectomy alters bile release dynamics from pulsatile meal-stimulated to continuous, and results in retrograde duodeno-gastric bile reflux (DGR). Bile is implicated in mucosal injury after gastric surgery, but whether cholecystectomy causes esophagogastric mucosal inflammation, therefore increasing the risk of metaplasia, is unclear.
This study examined whether cholecystectomy-induced DGR promotes chronic inflammatory mucosal changes of the stomach and/or the esophagogastric junction (EGJ). Four groups of patients were studied and compared with controls. A group of patients was studied before and 1 year after cholecystectomy; 2 further groups were studied long-term post-cholecystectomy (LTPC) at 5 to 10 years and 10 to 20 years. All underwent abdominal ultrasound and upper gastrointestinal endoscopy with gastric antral and EGJ biopsies, noting the presence of gastric bile pooling. Biopsy specimens were stained for Ki67 and p53 overexpression, and the bile reflux index (BRI) was calculated.
At endoscopy, bile pooling was observed in 9 of 26 (34.6%) controls, in 8 of 25 (32%) patients pre-cholecystectomy, in 15 of 25 (60%) 1 year post-cholecystectomy patients (p = 0.047), and 23 of 29 (79.3%) LTPC patients (p = 0.001). Bile reflux index positivity at the EGJ increased from 19% of controls through 41% of LTPC patients (p = 0.032). Ki67 was overexpressed at the EGJ in 19% of controls, but in 62% of LTPC patients (p = 0.044); p53 was overexpressed at the EGJ in 19% of controls compared with 66% of LTPC patients (p = 0.001).
Duodeno-gastric bile reflux was more common in patients with gallstones than in controls, and its incidence doubled after cholecystectomy. This was associated with inflammatory changes in the gastric antrum and the EGJ, evident in most LTPC patients. Ki67 and p53 overexpression at the EGJ suggests cellular damage attributable to chronic bile exposure post-cholecystectomy, increasing the likelihood of dysplasia. Further studies are required to determine whether DGR-mediated esophageal mucosal injury is reversible or avoidable, and whether surveillance endoscopy is indicated after cholecystectomy.
Copyright Â© 2016 American College of Surgeons. Published by Elsevier Inc. All rights reserved.