Practice Essentials
The term postcholecystectomy syndrome (PCS) describes the presence of symptoms after cholecystectomy. [1, 2] 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. [3] 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.
Pathophysiology and Etiology
Bile is thought to be the cause of PCS in patients with mild gastroduodenal symptoms or diarrhea. [4] 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 [5] |
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%). [6] 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.
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. [7] 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. [8] 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. [9] Russello found 30% of patients with postcholecystectomy symptoms, 13% with PCS, and 10% with the same preoperative symptoms. [10] Anand had 18% of patients with symptoms (24 mild, 7 severe). [11] Freud found that 62% of patients had less severe symptoms than preoperatively, 31% had the same symptoms, and 7% had more severe symptoms. [12]
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. [12] 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.
A study (N = 275) using data from the National Inpatient Sample (NIS) database found the incidence of PCS to be 5.5% in those aged 10-19 years, 13.8% in those aged 20-29 years, 20.0% in those aged 30-39 years, 16.7% in those aged 40-49 years, 15.6% in those aged 50-59 years, 14.9% in those aged 60-69 years, 7.3% in those aged 70-79 years, and 6.2% in those aged 80 years or older. [13]
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. [14] 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%.
Tables
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 [5] |
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 |
