Postcholecystectomy Syndrome
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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.
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
Trauma
Cyst
Malignancy and cholangiocarcinoma
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
Pancreatic stone
Pancreatic cysts
Benign tumors
Esophagus
Aerophagia
Achalasia
Stomach
Bile gastritis
Peptic ulcer disease
Gastric cancer
Duodenum
Adhesions
Small bowel
Adhesions
Incisional hernia
Colon [4]
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
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.
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:
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.
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.
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%.
Womack NA, Crider RL. The persistence of symptoms following cholecystectomy. Ann Surg. 1947 Jul. 126(1):31-55. [Medline].
Walters JR, Tasleem AM, Omer OS, Brydon WG, Dew T, le Roux CW. A new mechanism for bile acid diarrhea: defective feedback inhibition of bile acid biosynthesis. Clin Gastroenterol Hepatol. 2009 Nov. 7 (11):1189-94. [Medline].
Zollinger R. Observations following distention of the gallbladder and common duct in man. Proc Soc Exper Biol & Med. 1922-23. 30:1260-1.
Siddiqui AA, Kedika R, Mahgoub A, Patel M, Cipher DJ, Bapat V. A previous cholecystectomy increases the risk of developing advanced adenomas of the colon. South Med J. 2009 Nov. 102 (11):1111-5. [Medline].
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].
McHardy C. Postcholecystectomy syndrome. Disease-A-Month. 1959. 1:1-40.
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].
Schoenemann J, Zeidler J. [Sequelae of cholecystectomy]. Z Gastroenterol. 1997 Feb. 35(2):139-45. [Medline].
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].
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].
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].
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].
Filip M, Saftoiu A, Popescu C, Gheonea DI, Iordache S, Sandulescu L, et al. Postcholecystectomy syndrome – an algorithmic approach. J Gastrointestin Liver Dis. 2009 Mar. 18 (1):67-71. [Medline]. [Full Text].
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].
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].
Sakai Y, Tsuyuguchi T, Ishihara T, Sugiyama H, Miyakawa K, Yukisawa S, 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].
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].
Mahid SS, Jafri NS, Brangers BC, Minor KS, Hornung CA, Galandiuk S. 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].
Coté GA, Ansstas M, Shah S, Keswani RN, Alkade S, Jonnalagadda SS, et al. Findings at endoscopic retrograde cholangiopancreatography after endoscopic treatment of postcholecystectomy bile leaks. Surg Endosc. 2010 Jul. 24 (7):1752-6. [Medline].
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
Trauma
Cyst
Malignancy and cholangiocarcinoma
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
Pancreatic stone
Pancreatic cysts
Benign tumors
Esophagus
Aerophagia
Achalasia
Stomach
Bile gastritis
Peptic ulcer disease
Gastric cancer
Duodenum
Adhesions
Small bowel
Adhesions
Incisional hernia
Colon [4]
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
20% organ other than hepatobiliary or pancreatic
Foreign bodies, including gallstones and surgical clips
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
Disclosure: Nothing to disclose.
John Geibel, MD, DSc, MSc, AGAF Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow
John Geibel, MD, DSc, MSc, AGAF 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: Nothing to disclose.
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.
Postcholecystectomy Syndrome
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