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Postcholecystectomy Syndrome

  • Author: Steen W Jensen, MD; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
 
Updated: Dec 16, 2015
 

Background

The term postcholecystectomy syndrome (PCS) describes the presence of symptoms after cholecystectomy.[1] These symptoms can represent either the continuation of symptoms thought to be caused by gallbladder pathology or the development of new symptoms normally attributed to the gallbladder. PCS also includes the development of symptoms caused by removal of the gallbladder (eg, gastritis and diarrhea).

In general, PCS is a preliminary diagnosis and should be renamed with respect to the disease identified by an adequate workup. It arises from alterations in bile flow due to loss of the reservoir function of the gallbladder. Two types of problems may arise. The first is continuously increased bile flow into the upper gastrointestinal (GI) tract, which may contribute to esophagitis and gastritis. The second is related to the lower GI tract, where diarrhea and colicky lower abdominal pain may result.[2] This article mainly addresses the general issues of PCS.

PCS reportedly affects about 10-15% of patients. In the author’s experience, PCS has occurred in 14% of patients. Effective communication between patients and their physicians, with specific inquiry directed at eliciting frequently anticipated postoperative problems, may be necessary to reveal the somewhat subtle symptoms of PCS.

Treatment should be governed by the specific diagnosis made and may include pharmacologic or surgical approaches.

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Pathophysiology and Etiology

Bile is thought to be the cause of PCS in patients with mild gastroduodenal symptoms or diarrhea.[3] Removal of the reservoir function of the gallbladder alters bile flow and the enterohepatic circulation of bile. The pathophysiology of PCS is related to alterations in bile flow and is not yet fully understood.

Early articles on PCS focused primarily on anatomic abnormalities that were grossly or microscopically identifiable at the time of exploratory surgery. Improvements in technology and imaging studies have yielded an improved understanding of biliary tract disorders. This has affected the preoperative workup of patients with suspected gallbladder disease as well as those with PCS, making functional disorders of the biliary tract (including irritable sphincter) the most common causes of PCS (see Table 1 below).

Table 1. Etiologies of Postcholecystectomy Syndrome by Anatomic Location (Open Table in a new window)

Anatomy Etiology
Gallbladder remnant and cystic duct Residual or reformed gallbladder



Stump cholelithiasis



Neuroma



Liver Fatty infiltration of liver



Hepatitis



Hydrohepatosis



Cirrhosis



Chronic idiopathic jaundice



Gilbert disease



Dubin-Johnson syndrome



Hepatolithiasis



Sclerosing cholangitis



Cyst



Biliary tract Cholangitis



Adhesions



Strictures



Trauma



Cyst



Malignancy and cholangiocarcinoma



Obstruction



Choledocholithiasis



Dilation without obstruction



Hypertension or nonspecific dilation



Dyskinesia



Fistula



Periampullary Sphincter of Oddi dyskinesia, spasm, or hypertrophy



Sphincter of Oddi stricture



Papilloma



Cancer



Pancreas Pancreatitis



Pancreatic stone



Pancreatic cancer



Pancreatic cysts



Benign tumors



Esophagus Aerophagia



Diaphragmatic hernia



Hiatal hernia



Achalasia



Stomach Bile gastritis



Peptic ulcer disease



Gastric cancer



Duodenum Adhesions



Duodenal diverticula



Irritable bowel disease



Small bowel Adhesions



Incisional hernia



Irritable bowel disease



Colon[4] Constipation



Diarrhea



Incisional hernia



Irritable bowel disease



Vascular Intestinal angina



Coronary angina



Nerve Neuroma



Intercostal neuralgia



Spinal nerve lesions



Sympathetic imbalance



Neurosis



Psychic tension or anxiety



Bone Arthritis
Other Adrenal cancer



Thyrotoxicosis



20% organ other than hepatobiliary or pancreatic



Foreign bodies, including gallstones and surgical clips



Abu Farsakh et al found gastritis to be more frequent postoperatively (30% vs 50%).[5] Preoperatively, no cases of peptic ulcer disease (PUD) occurred, but three cases developed postoperatively. It was also shown that fasting gastric bile acid concentration increased after cholecystectomy, and the increase was greater in patients with PCS.

At exploratory surgery, 8% of patients remain without a diagnosis.

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Epidemiology

United States statistics

During the late 1990s, approximately 500,000-600,000 cholecystectomies were performed each year in the United States; most of them were laparoscopic. With at least 10% of patients developing PCS, approximately 50,000 or more cases of PCS occur each year. Study-to-study variability is great. PCS is reported to have been found in 5-30% of patients, with 10-15% being the most reasonable range.

McHardy found that 7.5% of patients with PCS required hospitalization.[6] The international incidence of PCS is almost identical to that in the United States.

Peterli found that 65% of patients had no symptoms, 28% had mild symptoms, 5% had moderate symptoms, and 2% had severe symptoms.[7] Peterli also found that PCS was caused by functional disorders in 26% of patients, peptic disease in 4%, wound pain in 2.4%, stones in 1%, subhepatic fluid in 0.8%, and incisional hernia in 0.4%.

Schoenemann found that functional disorders were the most common cause of PCS.[8] Russello found 30% of patients with postcholecystectomy symptoms, 13% with PCS, and 10% with the same preoperative symptoms.[9] Anand had 18% of patients with symptoms (24 mild, 7 severe).[10] Freud found that 62% of patients had less severe symptoms than preoperatively, 31% had the same symptoms, and 7% had more severe symptoms.[11]

In the author’s experience, a 14% risk of PCS exists among all patients, and the risk of PCS has not been associated with any preoperative finding.

It should be noted that about 50% of patients with a preoperative psychiatric disorder have an organic cause of PCS, whereas only 23% of patients without a psychiatric disorder have an organic cause.

Numerous researchers have attempted to develop preoperative risk stratification. No full consensus has been reached, but many would agree that a proper preoperative workup and skilled surgery should include complete evaluation of the extrahepatic biliary tree. Some risk stratification summaries follow:

  • An urgent operation puts patients at a higher risk for developing PCS
  • If the procedure is performed for stones, 10-25% of patients develop PCS; if no stones are present, 29% of patients develop PCS
  • If the duration of symptoms before surgery is less than 1 year, 15.4% of patients develop PCS; if preoperative symptom duration is 1-5 years, 21% develop PCS; if preoperative symptom duration is 6-10 years, 31% develop PCS; and if preoperative symptom duration is more than 10 years, 34% develop PCS
  • If a choledochotomy is performed, 23% of patients develop PCS; if choledochotomy is not performed, 19% develop PCS

Some researchers have found the incidence of PCS to be the same, regardless of typical or atypical preoperative symptoms. Previous surgery, bile spill, and stone spill did not make a difference in the incidence of PCS.

Age- and sex-related demographics

Freud found age and sex differences.[11] Patients aged 20-29 years had an incidence of 43%; those aged 30-39 years, 27%; those aged 40-49 years, 21%; those aged 50-59 years, 26%; and those aged 60-69 years, 31%. Patients older than 70 years did not develop PCS. Females had a 28% incidence of PCS, and males had a 15% incidence.

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Prognosis

Outcome and prognosis vary in accordance with the variety of patients and conditions encountered and the operations that may be performed.

Moody showed that 75% of his patients had good-to-fair relief of pain on long-term follow-up.[12] Short-term complications are common (5-40%). Hyperamylasemia is the most common complication but usually resolves by postoperative day 10. Pancreatitis is expected in 5% of cases and death in 1%.

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Contributor Information and Disclosures
Author

Steen W Jensen, MD Chief, Department of Surgery, Plumas District Hospital

Steen W Jensen, MD is a member of the following medical societies: American College of Surgeons, California Medical Association

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Acknowledgements

Amy L Friedman, MD Professor of Surgery, Director of Transplantation, State University of New York Upstate Medical University College of Medicine, Syracuse

Amy L Friedman, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Medical Women's Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, American Society of Transplantation, Association for Academic Surgery, Association of Women Surgeons, International College of Surgeons, International Liver Transplantation Society, NewYork Academy of Sciences, Pennsylvania Medical Society, Philadelphia County Medical Society, Society of Critical Care Medicine, and Transplantation Society

Disclosure: Nothing to disclose.

Oscar Joe Hines, MD Assistant Professor, Department of Surgery, University of California at Los Angeles School of Medicine

Oscar Joe Hines, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Endocrine Surgeons, American College of Surgeons, Association for Academic Surgery, Society for Surgery of the Alimentary Tract, and Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Acknowledgments

The author wishes to thank Gail Stentzel for her assistance with organization and data collection.

References
  1. Womack NA, Crider RL. The persistence of symptoms following cholecystectomy. Ann Surg. 1947 Jul. 126(1):31-55. [Medline].

  2. Walters JR, Tasleem AM, Omer OS, et al. A new mechanism for bile acid diarrhea: defective feedback inhibition of bile acid biosynthesis. Clin Gastroenterol Hepatol. 2009 May 6. [Medline].

  3. Zollinger R. Observations following distention of the gallbladder and common duct in man. Proc Soc Exper Biol & Med. 1922-23. 30:1260-1.

  4. Siddiqui AA, Kedika R, Mahgoub A, et al. A previous cholecystectomy increases the risk of developing advanced adenomas of the colon. South Med J. 2009 Nov. 102(11):1111-5. [Medline].

  5. Abu Farsakh NA, Stietieh M, Abu Farsakh FA. The postcholecystectomy syndrome. A role for duodenogastric reflux. J Clin Gastroenterol. 1996 Apr. 22(3):197-201. [Medline].

  6. McHardy C. Postcholecystectomy syndrome. Disease-A-Month. 1959. 1:1-40.

  7. Peterli R, Merki L, Schuppisser JP, Ackermann C, Herzog U, Tondelli P. [Postcholecystectomy complaints one year after laparoscopic cholecystectomy. Results of a prospective study of 253 patients]. Chirurg. 1998 Jan. 69(1):55-60. [Medline].

  8. Schoenemann J, Zeidler J. [Sequelae of cholecystectomy]. Z Gastroenterol. 1997 Feb. 35(2):139-45. [Medline].

  9. Russello D, Di Stefano A, Scala R, Favetta A, Emmi S, Guastella T, et al. Does cholecystectomy always resolve biliary disease?. Minerva Chir. 1997 Dec. 52(12):1435-9. [Medline].

  10. Anand AC, Sharma R, Kapur BM, Tandon RK. Analysis of symptomatic patients after cholecystectomy: is the term post-cholecystectomy syndrome an anachronism?. Trop Gastroenterol. 1995 Apr-Jun. 16(2):126-31. [Medline].

  11. Freud M, Djaldetti M, deVries A, Leffkowitz M. Postcholecystectomy syndrome: a survey of 114 patients after biliary tract surgery. Gastroenterologia. 1960. 93:288-93. [Medline].

  12. Moody FG, Vecchio R, Calabuig R, Runkel N. Transduodenal sphincteroplasty with transampullary septectomy for stenosing papillitis. Am J Surg. 1991 Feb. 161(2):213-8. [Medline].

  13. Filip M, Saftoiu A, Popescu C, et al. Postcholecystectomy syndrome - an algorithmic approach. J Gastrointestin Liver Dis. 2009 Mar. 18(1):67-71. [Medline]. [Full Text].

  14. Coelho-Prabhu N, Baron TH. Assessment of need for repeat ERCP during biliary stent removal after clinical resolution of postcholecystectomy bile leak. Am J Gastroenterol. 2010 Jan. 105(1):100-5. [Medline].

  15. Redwan AA. Multidisciplinary approaches for management of postcholecystectomy problems (surgery, endoscopy, and percutaneous approaches). Surg Laparosc Endosc Percutan Tech. 2009 Dec. 19(6):459-69. [Medline].

  16. Sakai Y, Tsuyuguchi T, Ishihara T, et al. The usefulness of endoscopic transpapillary procedure in post-cholecystectomy bile duct stricture and post-cholecystectomy bile leakage. Hepatogastroenterology. 2009 Jul-Aug. 56(93):978-83. [Medline].

  17. Phillips MR, Joseph M, Dellon ES, Grimm I, Farrell TM, Rupp CC. Surgical and endoscopic management of remnant cystic duct lithiasis after cholecystectomy--a case series. J Gastrointest Surg. 2014 Jul. 18(7):1278-83. [Medline].

  18. Mahid SS, Jafri NS, Brangers BC, et al. Meta-analysis of cholecystectomy in symptomatic patients with positive hepatobiliary iminodiacetic acid scan results without gallstones. Arch Surg. 2009 Feb. 144(2):180-7. [Medline].

  19. Cote GA, Ansstas M, Shah S, et al. Findings at endoscopic retrograde cholangiopancreatography after endoscopic treatment of postcholecystectomy bile leaks. Surg Endosc. 2009 Dec 30. [Medline].

 
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Table 1. Etiologies of Postcholecystectomy Syndrome by Anatomic Location
Anatomy Etiology
Gallbladder remnant and cystic duct Residual or reformed gallbladder



Stump cholelithiasis



Neuroma



Liver Fatty infiltration of liver



Hepatitis



Hydrohepatosis



Cirrhosis



Chronic idiopathic jaundice



Gilbert disease



Dubin-Johnson syndrome



Hepatolithiasis



Sclerosing cholangitis



Cyst



Biliary tract Cholangitis



Adhesions



Strictures



Trauma



Cyst



Malignancy and cholangiocarcinoma



Obstruction



Choledocholithiasis



Dilation without obstruction



Hypertension or nonspecific dilation



Dyskinesia



Fistula



Periampullary Sphincter of Oddi dyskinesia, spasm, or hypertrophy



Sphincter of Oddi stricture



Papilloma



Cancer



Pancreas Pancreatitis



Pancreatic stone



Pancreatic cancer



Pancreatic cysts



Benign tumors



Esophagus Aerophagia



Diaphragmatic hernia



Hiatal hernia



Achalasia



Stomach Bile gastritis



Peptic ulcer disease



Gastric cancer



Duodenum Adhesions



Duodenal diverticula



Irritable bowel disease



Small bowel Adhesions



Incisional hernia



Irritable bowel disease



Colon[4] Constipation



Diarrhea



Incisional hernia



Irritable bowel disease



Vascular Intestinal angina



Coronary angina



Nerve Neuroma



Intercostal neuralgia



Spinal nerve lesions



Sympathetic imbalance



Neurosis



Psychic tension or anxiety



Bone Arthritis
Other Adrenal cancer



Thyrotoxicosis



20% organ other than hepatobiliary or pancreatic



Foreign bodies, including gallstones and surgical clips



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