Saturday, May 31, 2008

Post Cholecystectomy Syndrome (PCS)

Post Cholecystectomy Syndrome (PCS)

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. 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.

History of the Procedure
In 1947, Womack and Crider first described PCS, defining it as the presence of symptoms after cholecystectomy.1 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 Tc 99m–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.

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.2 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.3 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%.3

Schoenemann found that functional disorders were the most common cause of PCS.4
Russello found 30% of patients with postcholecystectomy symptoms, 13% with PCS, and 10% with the same preoperative symptoms.5

Anand had 18% of patients with symptoms (24 mild; 7 severe).6

Freud found that 62% of patients had less severe symptoms than preoperatively, 31% had the same symptoms, and 7% had more severe symptoms.7

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:
  1. An urgent operation puts patients at a higher risk for developing PCS.
  2. If the procedure is performed for stones, 10-25% of patients develop PCS. If no stones are present, 29% of patients develop PCS.
  3. 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%.
  4. If a choledochotomy is performed, 23% of patients develop PCS; if choledochotomy is not performed, 19% develop PCS.
  5. Some researchers found that the incidence of PCS is the same regardless of typical or atypical preoperative symptoms.
  6. Prior surgery, bile spill, and stone spill did not make a difference in the incidence of PCS.
  7. Freud found age and sex differences.7 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.
  8. 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. 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%).8 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.

Etiologies of Postcholecystectomy Syndrome by Anatomical Location

Anatomy........................Etiology
_____________________________________________________
Gallbladder remnant and......Residual or reformed gallbladder
cystic duct......................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 herniaAchalasia

Stomach.........................Bile gastritis
...................................PUD
...................................Gastric cancer

Duodenum.......................Adhesions
...................................Duodenal diverticula
...................................Irritable bowel disease

Small bowel.....................Adhesions
...................................Incisional hernia
...................................Irritable bowel disease

Colon............................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.

Clinical
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%.7
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.

WORKUP

Lab Studies
The workup for PCS varies. An extensive study of the patient should be performed in an attempt to identify a specific cause for the symptoms and to exclude serious postcholecystectomy complications. Surgical reexploration should be considered a last resort.
Patient examination starts with a thorough history and physical (H&P) examination, with close scrutiny of the old record.

Particular attention should be paid to the preoperative workup and diagnosis, the surgical findings and pathologic examination, and any postoperative problems.

Discrepancies may lead to the diagnosis.

Additional workup is directed at the most likely diagnosis while excluding others.
Initial laboratory studies in the workup for PCS usually include a CBC to screen for infectious etiologies, a basic metabolic panel (BMP) and amylase to screen for pancreatic disease, a hepatic function panel (HFP) and prothrombin time (PT) to screen for possible liver or biliary tract diseases, and, if the patient is acutely ill, a blood gas analysis. If laboratory findings are within reference ranges, consider repeating these studies when symptoms are present.
Other laboratory studies that may be indicated include lipase, gamma-glutamyl transpeptidase (GGT), hepatitis panel, thyroid function, and cardiac enzymes.

Imaging Studies
A chest radiograph to screen for lower lung, diaphragmatic, and mediastinal diseases should be performed, along with abdominal films in most cases.

In patients with a history of back problems or arthritis, a lower dorsal spine series should also be obtained.

For patients with right upper quadrant (RUQ) pain, barium swallow, upper GI (UGI), and small bowel follow-through (SBFT) studies will evaluate the intestinal tract for evidence of esophagitis, including gastroesophageal reflux disease (GERD) and PUD. These studies are not always performed because esophagogastroduodenoscopy (EGD) is more reliable at identifying these diseases and also permits direct visualization of the ampulla of Vater.

An ultrasound study is almost always performed because it is a quick, noninvasive, and relatively inexpensive way to evaluate the liver, biliary tract, pancreas, and surrounding areas.
A 10- to 12-mm dilation of the common bile duct (CBD) is commonly observed.
Dilation of more than 12 mm is often diagnostic of distal obstruction, such as a retained stone, CBD stricture, or ampullary stenosis.

A CT scan can be helpful in identifying chronic pancreatitis or pseudocysts in patients with alcoholism or those with a history of pancreatitis.

In patients who are not candidates for EGD and ERCP, a helical CT scan or MRCP may reveal the cause of PCS.

When the pain is lower in the abdomen, a barium enema should be performed.

Nuclear imaging may demonstrate a postoperative bile leak. Occasionally, a HIDA scan or similar scintigraphic study may show delayed emptying or prolonged half-time, but these studies do not have the resolution to identify dilation, stricture, and so on. Emptying delayed by more than 2 hours or prolonged half-time can help identify the sphincter of Oddi as a potential cause but cannot differentiate between stenosis and dyskinesia.

Other Tests
In addition to the H&P and review of the old record, an ECG should be performed to screen for coronary disease.

A stress test or Holter monitoring may be indicated by the findings from the H&P, laboratory tests, or ECG.

Provocation tests, such as the morphine-Prostigmin test for pain or the secretin stimulation for pancreatic duct dilatation, have not been widely accepted. The author has not found either test to be particularly helpful.

Diagnostic Procedures
  1. An EGD procedure can be very helpful in the workup of PCS.
  2. EGD is a good procedure to evaluate the mucosa for signs of disease from the esophagus through the duodenum.
  3. EGD also allows direct visualization of the ampulla of Vater.
  4. The most useful test in the diagnosis of PCS is ERCP.
    ERCP is unsurpassed in visualization of the ampulla, biliary, and pancreatic ducts. At least 50% of patients with PCS have biliary disease, and most of these patients' conditions are functional in nature.
    An experienced endoscopist can confirm this diagnosis in most of these patients and can also provide additional diagnostic studies, such as biliary and ampullary manometry.
    Delayed emptying can be observed during ERCP as well as with HIDA scan.
    The CBD should clear of contrast within 45 minutes. Biliary manometry is performed in patients sedated without narcotics with a perfusion catheter; a pull-through technique is used for sphincter manometry.
    The sphincter is 5-10 mm long, and normal pressures are less than 30 mm Hg.
    As technology improves, it will be easier to detect retrograde contractions or increased frequency of contractions (also called tachyoddia).
    At the time of ERCP, therapeutic maneuvers, such as stone extraction, stricture dilatation, or sphincterotomy for dyskinesia or sphincter of Oddi stenosis, can be performed.
  5. A total colonoscopy may reveal colitis, and biopsy of the terminal ileum may confirm Crohn disease.
  6. A percutaneous transhepatic cholangiogram (PTC) or MRCP may be of use in patients who are not candidates for or who fail in ERCP attempts.
  7. Angiography of suspected diseased vessels may lead to intervention for vascular disorders, such as coronary or intestinal angina.
TREATMENT
Medical therapy
Once a diagnosis has been established, treatment should proceed as indicated for that diagnosis.
Patients with irritable bowel disease may be helped with the use of bulking agents, antispasmodics, or sedatives. The irritable sphincter may respond to high-dose calcium channel blockers or nitrates, but evidence is not yet convincing.
Cholestyramine has been of help for patients with diarrhea alone.
Antacids, histamine 2 (H2) blockers, or proton pump inhibitors (PPIs) can occasionally provide relief for patients with GERD or gastritis symptoms. One study showed that lovastatin might provide at least some relief in up to 67% of patients.
For patients with dyspeptic symptoms, Abu Farsakh and colleagues showed that symptoms correlate with gastric bile salt concentration.8

Surgical therapy
As with medical therapy, surgical therapy should be directed at the specific diagnosis.

The most commonly used procedure is ERCP. ERCP is both a diagnostic and a therapeutic procedure.

Surgery is indicated when an identifiable cause of PCS that responds well to operative intervention has been established.

Exploratory surgery is a last resort in the patient without a diagnosis and whose condition proves refractory to medical therapy.

In 1947, Womack suggested resection of scar and nerve tissue around the cystic duct stump.1 Others suggested resection of neuroma, cystic duct remnant, sphincter dilation sphincterotomy sphincteroplasty, biliary bypass, common bile duct exploration (CBDE), and stone removal. With ERCP, most of these diagnoses would have been ruled out or treated, and the idea of amputation of neuroma was controversial.

Patients abusing alcohol or narcotics are especially difficult to manage, and exploratory surgery should be postponed until they have stopped abusing these drugs.

A few patients have no identifiable causes and an unrevealing exploration that may respond to sphincteroplasty, including the bile and pancreatic ducts. This group of patients is not yet identifiable preoperatively.

If, after a complete evaluation (including an ERCP with sphincterotomy), a patient continues to have debilitating, intermittent RUQ pain, and no diagnosis is found, the procedure of choice after a normal exploratory laparotomy is a transduodenal sphincteroplasty.

Preoperative details
After workup, the patient should be made safe for an operation, and the planned operation should be safe for the patient.

The endoscopist should be experienced in evaluating this type of patient, and the surgeon should be experienced in operating on them. A skilled assistant should also be invited, and the radiologist and endoscopist involved in the case should be available for consultation.
The patient should be the first and only individual undergoing surgery in the morning. A fresh team in the operating room is more helpful in a potentially long and tedious case.

Intraoperative details
As with all operations, the patient should be safe to operate upon, and the surgery should be safe for the patient. The operation should follow a logical and systematic course with attention to detail and careful handling of tissues, especially those of the biliary tract.

After exploration and lysis of adhesions, perform an interoperative cholangiogram (IOC). The only circumstance in which IOC may be omitted is when a nonbiliary source is identified and there is a high-quality preoperative cholangiogram, such as from ERCP.

Womack and others have suggested resection of scar and nerve tissue around the cystic duct stump, although this method is controversial.1

Most authorities agree that a sphincteroplasty and septoplasty between the CBD and pancreatic duct should be performed unless the head of the pancreas is hard, fibrotic, or indurated from chronic pancreatitis. In this situation, choledochoduodenostomy may prove more effective. Sphincteroplasty requires a generous right subcostal incision and mobilization of the hepatic flexure of the colon and the duodenum.

The portal structures are identified, along with the cystic duct stump. When possible, perform an IOC through the stump. Choledochoscopy may also be helpful if a stone or potentially malignant stricture was identified. This can also be accomplished via the cystic duct stump. Ligate the stump with absorbable suture within 5 mm of the CBD junction when no longer needed. If the stump is not used, place a T-tube through the choledochotomy when done.

A short duodenotomy is made, centered over the ampulla, and fine silk stay sutures are placed. A small biliary catheter should be placed, either antegrade or retrograde.

With 12 o'clock being cephalad and 9 o'clock posterior, make a 3- to 5-mm incision at 11 o'clock through the ampulla over the catheter. Place fine monofilament absorbable sutures approximating the duodenal and CBD mucosa. This should continue along the catheter for 2-3 cm, using fine Potts scissors. Lachrymal probes can be used to ensure that the pancreatic duct is not ligated.

Secretin (1-2 U IV) can be administered to help identify the location of the pancreatic duct. A septoplasty is then carried out in a similar fashion for approximately 1 cm.

The result should be the easy passage of a 5-mm probe into the CBD and a 2-mm probe into the pancreatic duct. Take biopsies as needed.

The duodenum is closed in 2 layers. A T-tube is left whenever a choledochotomy is created.

Postoperative details
Postoperative care should be appropriate for the patient and the operation that was performed.


Follow-up care should be appropriate for the patient and the operation that was performed.

COMPLICATIONS

Short-term complications are common (5-40%).

  1. Hyperamylasemia is most common but usually resolves by the 10th postoperative day.
  2. Pancreatitis is expected in 5% of cases and death in 1%.
  3. Moody showed that 75% of his patients had good-to-fair relief of pain on long-term follow-up.9
OUTCOME AND PROGNOSIS
Outcome and prognosis vary in accordance with the variety of patients and conditions encountered and the operations that may be performed.

FUTURE AND CONTROVERSIES

As technology and understanding of the functional disorders of the GI and biliary tracts improve, the ability to make a diagnosis and to treat discovered illnesses will improve. PCS will be a less frequent diagnosis as patients are more efficiently screened and evaluated and as specific diagnoses are confirmed.

ACKNOWLEDGMENTS
Gail Stentzel for her help in keeping me organized and in assisting with data collection. Jan, my wife, for her love and patience.

REFERENCES

  1. Womack NA, Crider RL. The persistence of symptoms following cholecystectomy. Ann Surg. Jul 1947;126(1):31-55. [Medline].
  2. McHardy C. Postcholecystectomy syndrome. Disease-A-Month. 1959;1:1-40.
    Peterli R, Merki L, Schuppisser JP, Ackermann C, Herzog U, Tondelli P.
  3. [Postcholecystectomy complaints one year after laparoscopic cholecystectomy. Results of a prospective study of 253 patients]. Chirurg. Jan 1998;69(1):55-60. [Medline].
  4. Schoenemann J, Zeidler J. [Sequelae of cholecystectomy]. Z Gastroenterol. Feb 1997;35(2):139-45. [Medline].
  5. Russello D, Di Stefano A, Scala R, Favetta A, Emmi S, Guastella T, et al. Does cholecystectomy always resolve biliary disease?. Minerva Chir. Dec 1997;52(12):1435-9. [Medline].
  6. Anand AC, Sharma R, Kapur BM, Tandon RK. Analysis of symptomatic patients after cholecystectomy: is the term post-cholecystectomy syndrome an anachronism?. Trop Gastroenterol. Apr-Jun 1995;16(2):126-31. [Medline].
  7. 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].
  8. Abu Farsakh NA, Stietieh M, Abu Farsakh FA. The postcholecystectomy syndrome. A role for duodenogastric reflux. J Clin Gastroenterol. Apr 1996;22(3):197-201. [Medline].
  9. Moody FG, Vecchio R, Calabuig R, Runkel N. Transduodenal sphincteroplasty with transampullary septectomy for stenosing papillitis. Am J Surg. Feb 1991;161(2):213-8. [Medline].
  10. Bartlett MK, Quinby WC Jr. Surgery of the biliary tract. III. Secondary operations of the
  11. common bile duct. NEJM. 1957;256:11.
  12. Bensen KW. Dialation of bile ducts and its relation to distress after cholecystectomy. Am J Digest. 1940;7:1-2.
  13. Berk JE. General considerations of gall bladder and biliary tract disorders. Disturbances in Gastrointestinal Motility. 1959;123.
  14. Berk JE, Lee RN. Intravenous cholangiography in detection of stone bearing cystic-duct remnants (so-called re-formed gallbladders). Am J Digest Dis. 1958;3:220.
  15. Beye HL. Conditions necessitating surgery after cholecystectomy. S G & O. 1936;62:191-202.
  16. Boren JA, Walter W. Strictures of the bile ducts and their treatment. Proc Staff Meet Mayo Clin. Jun 15 1955;30(12):245-52. [Medline].
  17. Butsch WL, McGowan JM, Walters W. Clinical studies on the influence of certain drugs in relation to biliary pain and to the variations in intrabiliary pressure. S G & O. 1936;63:451-6.
  18. Cattel RB, Braasch JW. Strictures of the bile duct. S Clin NA. 1958;38:645.
  19. Cattel RB, Colcock BP, Pollack JL. Stenosis of the sphincter of oddi. NEJM. 1957;256:429.
  20. Chernov VN, Khimichev VG, Temchurin ShA. [The postcholecystectomy syndrome and its prevention]. Khirurgiia (Mosk). 1996;(6):57-60. [Medline].
  21. Coakley FV, Schwartz LH, Blumgart LH, Fong Y, Jarnagin WR, Panicek DM. Complex postcholecystectomy biliary disorders: preliminary experience with evaluation by means of breath-hold MR cholangiography. Radiology. Oct 1998;209(1):141-6. [Medline].
  22. Davis L, Hart JT, Crain RC. The pathway for visceral impulses within the spinal cord. S G & O. 1929;48:647-51.
  23. Debray C, Roux M, LeCanuet R. Late results of 300 cholecystectomies performed with the aid of preoperative radiomanometery. Semaine Hop Paris. 1960;36:296.
  24. Dimonte M, Calabrese R. [Post-cholecystectomy syndrome: hepatobiliary scintigraphy and cholangiopancreatography with magnetic resonance in 5 consecutive patients. Comparison of results and integrated diagnosis]. Radiol Med (Torino). Dec 1998;96(6):588-91. [Medline].
  25. Donaldson GA, Allen AW, Bartlett MK. Postoperative bile-duct strictures: their etiology and treatment. NEJM. 1956;254:50.
  26. Doubilet H, Colp R. Resistance of the sphincter in the human. S G & O. 1937;64:622-3.
  27. Doubilet H, Mulholland JH. Eight years of pancreatitis and sphincterotomy. JAMA. 1956;160:521.
  28. Doubilet H, Mulholland JH. Recurrent acute pancreatitis: observations on etiology and surgical treatment. Ann Surg. 1948;128:609.
  29. Dreiling DA. Studies in pancreatic function III. The use of secretin test in the diagnosis of patients with the postcholecystectomy syndrome. Gastroenterology. 1960;16:162.
  30. Dreiling, DA. The functional aspect of biliary colic persistent after cholecystectomy. The postcholecystectomy syndrome. 1962;7:603-12.
  31. Dubin IN. Chronic idiopathic jaundice. Am J Med. 1958;24:268.
  32. Elman R. Common problems in surgical diagnosis. S Clin NA. 1940;20:1247-60.
  33. Elman R. Surgical aspects of acute pancreatitis with special reference to it frequency as revealed by serum amylase. JAMA. 1942;118:1265.
  34. Evans PR, Bak YT, Shuter B, Hoschl R, Kellow JE. Gastroparesis and small bowel dysmotility in irritable bowel syndrome. Dig Dis Sci. Oct 1997;42(10):2087-93. [Medline].
  35. Evans PR, Dowsett JF, Bak YT, Chan YK, Kellow JE. Abnormal sphincter of Oddi response to cholecystokinin in postcholecystectomy syndrome patients with irritable bowel syndrome. The irritable sphincter. Dig Dis Sci. May 1995;40(5):1149-56. [Medline].
  36. Feldman M. Polycholecystectomy syndrome with special reference to the cystic duct remnant. Gastroenterology. 1958;34:239.
  37. Garlock JH, Hurwitt ES. The cystic duct stump syndrome. Surgery. 1951;29:833.
  38. Gieslak AK, Stout AP. Traumatic and amputation neuromas. Arch Surg. 1946;53:646.
  39. Glenn F, Johnson Jr G. Cystic duct remnant, a sequela of incomplete cholecystectomy. Surg Gynecol Obstet. Sep 1955;101(3):331-45. [Medline].
  40. Graham EA, Mackey WH. A consideration of the stoneless gallbladder. JAMA. 1934;103:1497-9.
  41. Gray HK, Garrett Jr CM. Obstruction of the duodenum beyond the ampulla of Vater; a possible cause of symptoms suggesting disease of the biliary tract. Ann Surg. Sep 1955;142(3):532-6. [Medline].
  42. Gray HK, Sharpe WS. Biliary dyskinesia: role played by remnant of cystic duct. Mayo Clinic. 1944;19:164-8.
  43. Grimson KS, Hesser FH, Kitchen WW. Early clinical results of transabdominal celiac and superior mesenteric ganglionectomy, vagotomy, or transthoracic splanchnicectomy in patients with chronic abdominal visceral pain. Surgery. 1947;22:230.
  44. Halligan EJ, Rohim F. Transcutaneous hepatic cholangiographic study: its importance in the diagnosis and management of biliary disease. J Int Coll Surg. Feb 1959;31(2):154-60. [Medline].
  45. Hase T, Kodama M, Shibata J, Kurumi Y, Kishida A, Kawaguchi A, et al. Three-dimensional helical computed tomography with intravenous cholangiography for sclerosing cholangitis manifested as postcholecystectomy symptom. J Clin Gastroenterol. Apr 1997;24(3):169-72. [Medline].
  46. Heffernon EW, Milhon WA, Roxen SW. Irritable colon and gallbladder disease. JAMA. 1960;173:1.
  47. Hicken NF, McAllister AH, Walker G. The problem of retained common duct stones. Am J Surg. 1959;97:173.
  48. Hicken NF, McAllister AJ, Call DW. Residual choledochal stones: etiology and complications in 110 cases. Arch Surg. 1954;68:643.
  49. Hicken NF, White LB, Coray QB. External biliary fistulas: a study of 23 cases. SG&O. 1942;74:828.
  50. Hinkel CL, Miller GA. Correlation of symptoms, age, sex, and habitus with cholecystographic findings in 1000 consecutive examinations. Gastroenterology. 1957;32:807.
  51. Imamoglu K, Perry Jr JF, Wangensteen OH. Experimental production of gallstones by incomplete stricture of the common bile duct. Surgery. 1957;42:623.
  52. Iszak FC. The postcholecystectomy syndrome: its prevention and treatment by choledochoduodenostomy. J Intern Coll Surg. 1958;30:802.
  53. Ivy AC, Sanbloom P. Biliary dyskinesia. Ann Int Med. 1934;8:115-22.
  54. Judd ES. Clinical versus pathologic cholecystitis. Coll Papers Mayo Clinic. 1925;17:152-6.
  55. Kaplan IW. Operative cholangiography. Am J Gastroenterology. 1955;23:547.
  56. Kourtas B, Tobler A. The postcholecystectomy syndrome on the basis of late results in 551 cases followed up during years 1950-1955. Chirug. 1959;30:398.
  57. Lamari TK, Fock G. Cystic duct remnant; a cause of biliary distress following incomplete cholecystectomy. Acta Chir Scandinav. 1958;114:361.
  58. Lester LJ, Colp R. Treatment of biliary dyskinesia with special reference to sphincterotomy. AMA Arch Surg. 1952;64:168.
  59. Madura JA, Madura JA 2nd, Sherman S, Lehman GA. Surgical sphincteroplasty in 446 patients. Arch Surg. May 2005;140(5):504-11; discussion 511-3. [Medline].
  60. McClenahan JE, Evans JA, Braunstein PW. Intravenous cholangiography in the post cholecystectomy syndrome. JAMA. 1955;159:1353.
  61. McHardy G. Postcholecystectomy syndrome disturbances in gastrointestinal motility. Springfield IL: Thomas; 1959:194.
  62. Mergener K, Clavien PA, Branch MS, Baillie J. A stone in a grossly dilated cystic duct stump: a rare cause of postcholecystectomy pain. Am J Gastroenterol. Jan 1999;9(1):229-31. [Medline].
  63. Meyers SG, Sandweiss DJ, Saltzstein HC. End results after gallbladder operations with analysis of causes of residual symptoms. Am J Digest Dis. 1938;5:667.
  64. Miller GH. The re-formed gallbladder. J OK MA. 1945;38:1.
  65. Mirizzi PL. La Cholangiografia Durante las Operaciones de la Vias iliares. Bol y Trab Soc. Cir De Buenos Aires. 1932;16:1133.
  66. Morton CB 2nd. Post-cholecystectomy symptoms from cystic duct remnants. Ann Surg. May 1954;139(5):679-82. [Medline].
  67. Mueler GP. The noncalculus gallbladder. JAMA. 1927;89:786-9.
  68. Pribam BOC. The method for dissolution of common duct stones remaining after operation. Surgery. 1947;142:1262.
  69. Pribram BOC. Postcholecystectomy syndromes. JAMA. 1942;40:1262.
  70. Puestow CB. Changes in intracholedochal pressure following cholecystectomy. SG&O. 1938;67:82-6.
  71. Raymer JB, Tarpinian DA, Myers SG. Symptoms following cholecystectomy. Am J Digest Dis. 1960;67:82-6.
  72. Ruffin J. Further observations on the use of 1131 labeled lipids in the study of disorders of the gastrointestinal tract. Gastroenterology. 1958;34:484.
  73. Sadah HA. Post-cholecystectomy biliary pain and dyspepsia. J OK State Med Assoc. 1994;87:316-8.
  74. Schrager VL, Ivy AC. Symptoms produced by distention of the gallbladder and biliary ducts. SG&O. 1928;47:1-13.
  75. Sherlock S. Diseases of the liver and biliary system. Charles C. Thomas, Publisher. 1955.
    Shingleton WM, Peete WPJ. The postcholecystectomy syndrome. Am Surg. 1962;28:19-31.
  76. Smioth ML, Santos M. Biliary radiomanometery. US Armed Forces MJ. 1959;8:481.
  77. Smith SW, Engel C, Averbook B. Problems of retained and recurrent common bile duct stones. JAMA. 1957;164:231.
  78. Snape WJ, Friedman MHF, Swenson PC. Correlation between cholecystogram and secretin test for gallbladder function. Am J M Sc. 1948;216:188.
  79. Walters W. Postcholecystectomy dyskinesia; with pancreatitis, sphincteritis, and choledocholithiasis as causes. J Am Med Assoc. Feb 11 1956;160(6):425-31. [Medline].
  80. Weir JF, Snell AM. Symptoms that persist after cholecystectomy. JAMA. 1935;105:1093-8.
  81. Westphal K. Muskelfunktion, nervensystem und pathologie der Gallenwege. Ztschr f klin Med. 1923;96:22-50.
  82. Whipple AO. Surgical criteria for cholecystectomy. Am J Surg. 1926;40:129-31.
  83. Wise RE, O'Brien RG. Interpretation of the intravenous cholangiogram. J Am Med Assoc. Mar 10 1956;160(10):819-27. [Medline].
  84. Womack NA, Siegert RB. Surgical aspects of lesions of Meckel's diverticulum. Ann Surg. Aug 1938;108(2):221-36. [Medline].
  85. Zollinger R. Observations following distention of the gallbladder and common duct in man. Proc Soc Exper Biol & Med. 1922-23;30:1260-1.
  86. Postcholecystectomy Syndrome excerpt

Article Last Updated: Jan 16, 2008


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