Postcholecystectomy Syndrome
- Author: Steen W Jensen, MD; Chief Editor: John Geibel, MD, DSc, MA more...
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 the gallbladder or the development of new symptoms normally attributed to the gallbladder. PCS also includes the development of symptoms caused by removal of the gallbladder.
In general, PCS is a preliminary diagnosis and should be renamed relevant to the disease identified by an adequate workup. PCS is caused by alterations in bile flow due to the loss of the reservoir function of the gallbladder. Two types of problems may arise. The first problem is continuously increased bile flow into the upper GI tract, which may contribute to esophagitis and gastritis. The second consequence 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 this 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.
Recent studies
In a retrospective study of 105 patients, Coté et al investigated whether follow-up endoscopic retrograde cholangiopancreatography (ERCP) and bile duct balloon sweeps are necessary to find abnormalities in patients who have undergone endoscopic treatment for postcholecystectomy bile duct leakage. Patients underwent an initial ERCP at the time of bile leak treatment and, after a mean interval of 6.9 weeks, a follow-up ERCP. At follow-up, 1 or more abnormalities were found in 27.6% of patients, including persistent bile leak, common bile duct (CBD) stones, and CBD sludge without stones. Balloon sweeps, administered to a subgroup of patients, revealed a 17.6% prevalence of CBD stones or sludge at follow-up.
The authors recommended that, owing to the prevalence of abnormalities after the endoscopic treatment of bile leaks, follow-up ERCP and balloon sweeps be performed in patients at the time of stent removal.[3]
History of the Procedure
In 1947, Womack and Crider first described PCS, defining it as the presence of symptoms after cholecystectomy.[4] These symptoms may actually represent either (1) the continuation of symptoms that had been interpreted as resulting from pathology of the gallbladder or (2) the development of new symptoms that might normally be attributed to the gallbladder. PCS is also the development of symptoms, such as gastritis and diarrhea, caused by removal of the gallbladder.
In the 1860s, cholecystotomy was the common surgical means of treating a diseased gallbladder. Cholecystectomy became routine about 20 years later. Cholecystectomy proved successful in treating the symptoms of biliary colic and cholecystitis in 80-95% of patients with stones. When stones were not present, the failure rate was as high as 40%.
In the 1920s, oral cholecystography (OCG), an important preoperative aid in the detection of stones or nonfunctioning gallbladders, was developed.
Since then, a wide variety of noninvasive imaging techniques have proven useful in the preoperative assessment of the gallbladder. Ultrasonography is the most accessible and cost-effective approach in most institutions.
Other noninvasive techniques include hepatobiliary scintigraphy with technetium-99m (99m Tc) – labeled iminodiacetic acid, otherwise known as a hepatoiminodiacetic acid (HIDA) scan with and without calculation of cholecystokinin (CCK)-stimulated ejection fraction (EF). Computed tomography (CT) scanning, helical or spiral CT scanning, and magnetic resonance cholangiopancreatography (MRCP) may be useful.
More invasive procedures that may prove valuable in defining the biliary anatomy include percutaneous transhepatic cholangiography (PTC) and endoscopic retrograde cholangiopancreatography (ERCP), with and without biliary and ampullary manometry and sphincterotomy. The intraoperative cholangiogram (IOC), along with a variety of different instrumentation methods, has been in use since the 1930s and has helped in the evaluation of the bile ducts at the time of surgery. These procedures have helped reduce the incidence of PCS because of better preoperative evaluation and diagnosis, especially in patients without stones.
Approximately 500,000-600,000 cholecystectomies were performed each year in the United States during the late 1990s, most of which were laparoscopic. With at least 10% of patients developing PCS, approximately 50,000 cases or more of PCS occur each year. Articles on PCS from the 1920s-1940s primarily focused on anatomical abnormalities that were grossly or microscopically identifiable at the time of exploratory surgery. With improvements in technology and imagining studies, our understanding of biliary tract disorders has improved. 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.
Problem
PCS is usually a temporary diagnosis. An organic or functional diagnosis is established in most patients after a complete workup. Many articles state that a complete preoperative evaluation is essential to minimizing this disease and that patients should be warned of the possibility of postoperative symptoms, which may start at any time from the immediate postoperative period to decades later. Many studies have also been performed in an attempt to identify those at increased risk for PCS and to develop a method of risk stratification. A large portion of data is inconsistent from study to study; however, the consensus opinion holds that the more secure the preoperative diagnosis, the lower the risk of PCS. Other reports find a cause for PCS in as many as 95% of patients.
Epidemiology
Frequency
- Study-to-study variability is great. PCS is 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.[5] 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.[6] 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.[7]
- Russello found 30% of patients with postcholecystectomy symptoms, 13% with PCS, and 10% with the same preoperative symptoms.[8]
- Anand had 18% of patients with symptoms (24 mild; 7 severe).[9]
- Freud found that 62% of patients had less severe symptoms than preoperatively, 31% had the same symptoms, and 7% had more severe symptoms.[10]
- 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.
- Many researchers have attempted to develop preoperative risk stratification. Consensus is limited, but 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 prior to surgery is less than 1 year, 15.4% of patients develop PCS; if the duration is 1-5 years, 21% develop PCS; if 6-10 years, 31%; and, if more than 10 years, 34%.
- If a choledochotomy is performed, 23% of patients develop PCS; if choledochotomy is not performed, 19% develop PCS.
- Some researchers found that the incidence of PCS is the same regardless of typical or atypical preoperative symptoms.
- Prior surgery, bile spill, and stone spill did not make a difference in the incidence of PCS.
- Freud found age and sex differences.[10] Patients aged 20-29 years had an incidence of 43%; those aged 30-39 years, 27%; 40-49 years, 21%; 50-59 years, 26%; and, 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.
- Note that half 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.
Etiology
Bile is thought to be the cause of PCS in patients with mild gastroduodenal symptoms or diarrhea.[11] Removal of the reservoir function of the gallbladder alters bile flow and the enterohepatic circulation of bile.
Abu Farsakh et al found gastritis to be more frequent postoperatively (30% vs 50%).[12] Preoperatively, no cases of peptic ulcer disease (PUD) occurred, but 3 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.
Table. Etiologies of Postcholecystectomy Syndrome by Anatomical 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 |
| Esophagus | Aerophagia Diaphragmatic hernia Hiatal hernia Achalasia |
| Stomach | Bile gastritis PUD Gastric cancer |
| Duodenum | Adhesions Duodenal diverticula Irritable bowel disease |
| Small bowel | Adhesions Incisional hernia Irritable bowel disease |
| Colon[13] | 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 |
Pathophysiology
The pathophysiology of PCS is related to alterations in bile flow and remains poorly understood.
Presentation
- A wide range of symptoms occurs. Symptoms are sometimes considered to be associated with the gallbladder.
- Freud found colic in 93% of patients, pain in 76%, jaundice in 24%, and fever in 38%.[10]
- In the author's patient population, the incidence of PCS is 14%. Pain is found in 71% of patients, diarrhea or nausea in 36%, and bloating or gas in 14%.
- The cause of PCS is identifiable in 95% of patients.
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| 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 |
| Esophagus | Aerophagia Diaphragmatic hernia Hiatal hernia Achalasia |
| Stomach | Bile gastritis PUD Gastric cancer |
| Duodenum | Adhesions Duodenal diverticula Irritable bowel disease |
| Small bowel | Adhesions Incisional hernia Irritable bowel disease |
| Colon[13] | 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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