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
View Table
See Table
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:
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.
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%.
A wide range of symptoms may be noted in patients with postcholecystectomy syndrome (PCS). 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%.[11] 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.
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 a careful physical 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 other possible causes.
Chest radiography should be performed to screen for lower-lung, diaphragmatic, and mediastinal diseases; in most cases, abdominal films should be obtained as well. 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 pain, barium swallow, upper gastrointestinal (GI), and small-bowel follow-through (SBFT) studies will evaluate the intestinal tract for evidence of esophagitis, including gastroesophageal reflux disease (GERD) and peptic ulcer disease (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. When the pain is lower in the abdomen, a barium enema should be performed.
Angiography of suspected diseased vessels may lead to intervention for vascular disorders, such as coronary or intestinal angina.
An ultrasonographic study is almost always performed; 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 exceeding 12 mm is often diagnostic of distal obstruction, such as a retained stone, CBD stricture, or ampullary stenosis.
In a study of 80 patients with PCS, Filip et al concluded that endoscopic ultrasonography (EUS) was a valuable tool for determining which patients require endoscopic retrograde cholangiopancreatography (ERCP).[13] The sensitivity and specificity of EUS were found to be 96.2% and 88.9%, respectively, in a subset of 53 patients who were ultimately diagnosed with biliary or pancreatic disease. The investigators found that the use of EUS helped to reduce the number of patients receiving ERCP by 51%.
EGD can be very helpful in the workup of PCS. It is a good procedure for evaluating the mucosa for signs of disease from the esophagus through the duodenum. EGD also allows direct visualization of the ampulla of Vater.
A total colonoscopy may reveal colitis, and biopsy of the terminal ileum may confirm Crohn disease.
ERCP is the most useful test in the diagnosis of PCS.[13, 14] It 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 hepatoiminodiacetic acid (HIDA) scanning. 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. Percutaneous transhepatic cholangiography (PTC) or magnetic resonance cholangiopancreatography (MRCP) may be of use in patients who are not candidates for ERCP or in whom ERCP has been unsuccessfully attempted.
Computed tomography (CT) 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.
Nuclear imaging may demonstrate a postoperative bile leak. Occasionally, a HIDA scan or similar scintigraphic study may show delayed emptying or a prolonged half-time, but these studies lack the resolution necessary to identify dilation, stricture, and so on. Emptying delayed by more than 2 hours or a prolonged half-time can help identify the sphincter of Oddi as a potential cause but cannot differentiate between stenosis and dyskinesia.
In addition to the history and physical examination and review of the old record, electrocardiography (ECG) should be performed to screen for coronary disease. A stress test or Holter monitoring may be indicated by the findings from the history and physical, laboratory tests, or ECG.
Provocation tests, such as the morphine-neostigmine test for pain or the secretin stimulation test for pancreatic duct dilatation, have not been widely accepted. The author has not found either test to be particularly helpful.
Postcholecystectomy syndrome (PCS) is usually a temporary diagnosis. An organic or functional diagnosis is established in most patients after a complete workup. Once a diagnosis has been established, treatment should proceed as indicated for that diagnosis. Treatment may be either medical or surgical.
Patients with irritable bowel syndrome may benefit from the administration of bulking agents, antispasmodics, or sedatives. The irritable sphincter may respond to high-dose calcium channel blockers or nitrates, but the available evidence is not yet convincing. Cholestyramine has been helpful for patients with diarrhea alone.
Antacids, histamine 2 (H2) blockers, or proton pump inhibitors (PPIs) can occasionally provide relief for patients with gastroesophageal reflux disease (GERD) or gastritis symptoms. One study showed that lovastatin might provide at least some relief in as many as 67% of patients.
For patients with dyspeptic symptoms, Abu Farsakh et al showed that symptoms correlated with gastric bile salt concentration.[5]
Like medical therapy, surgical therapy should be directed at the specific diagnosis.[15, 16] Surgery is indicated when an identifiable cause of PCS that is known to respond well to operative intervention has been established. The most commonly performed procedure is endoscopic retrograde cholangiopancreatography (ERCP), which can be both diagnostic and therapeutic. Exploratory surgery is a last resort in the patient who lacks 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, though this method is somewhat controversial.[1] Others suggested resection of neuroma, cystic duct remnant, sphincter dilation, sphincterotomy, sphincteroplasty, biliary bypass, common bile duct (CBD) exploration, 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.
In a few patients, no causes are identifiable and exploration is unrevealing, but the condition 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 ERCP with sphincterotomy), a patient continues to experience debilitating, intermittent right-upper-quadrant pain, and no diagnosis is found, the procedure of choice after a normal exploratory laparotomy is transduodenal sphincteroplasty.
When postcholecystectomy syndrome (PCS) results from remnant cystic duct lithiasis (RCDL; ie, gallstones within the cystic duct after cholecystectomy), endoscopic therapy may suffice, but surgical excision of the RCDL may be necessary in some cases.[17]
Procedural details
After workup, the patient should be made safe for an operation, and the planned operation should be safe for the patient. The operation should be structured to follow a logical and systematic course with attention to detail and careful handling of tissues, especially those of the biliary tract.
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 helpful in a potentially long and tedious case.
After exploration and lysis of adhesions, intraoperative cholangiography (IOC) should be performed. The only circumstance in which IOC may be omitted is when a nonbiliary source is identified and a high-quality preoperative cholangiogram is available (eg, from ERCP).
Most authorities agree that sphincteroplasty and septoplasty between the CBD and the 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, IOC should be performed 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. Once the stump is no longer needed, it is ligated with absorbable suture within 5 mm of the CBD junction. If the stump is not used, a T-tube should be placed through the choledochotomy when it is done.
A short duodenotomy is made, centered over the ampulla, and fine silk stay sutures are placed. A small biliary catheter should be placed in either an antegrade or a retrograde fashion.
With 12 o’clock representing cephalad and 9 o’clock posterior, a 3- to 5-mm incision is made at 11 o’clock through the ampulla over the catheter. Fine monofilament absorbable sutures are placed to approximate the duodenal and CBD mucosa. Placement 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 units intravenously) may 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 of a 2-mm probe into the pancreatic duct. Biopsy specimens may be taken as necessary.
The duodenum is closed in two layers. A T-tube is left whenever a choledochotomy is created. Postoperative care should be appropriate for the patient and the operation that was performed.
Many articles have stated that a complete preoperative evaluation is essential to minimizing the incidence of PCS and that patients should be warned of the possibility of symptoms after cholecystectomy, 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. To a large extent, the data are inconsistent from study to study; however, it is generally considered 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.
Since the development of oral cholecystography (OCG) in the 1920s as a preoperative aid in the detection of stones or nonfunctioning gallbladders, a wide variety of noninvasive imaging techniques have proven useful in preoperative gallbladder assessment. Ultrasonography is the most accessible and cost-effective approach in most institutions. Other noninvasive techniques include the following:
Hepatobiliary scintigraphy with technetium-99m (99mTc)-labeled iminodiacetic acid (ie, hepatoiminodiacetic acid [HIDA] scanning),[18] with and without calculation of cholecystokinin (CCK)-stimulated ejection fraction (EF)
Computed tomography (CT), including helical or spiral CT
Magnetic resonance cholangiopancreatography (MRCP)
More invasive procedures that may prove valuable in defining the biliary anatomy include the following:
Percutaneous transhepatic cholangiography (PTC) and ERCP, with and without biliary and ampullary manometry and sphincterotomy
IOC
These procedures have helped reduce the incidence of PCS by facilitating better preoperative evaluation and diagnosis, especially in patients without stones.
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 as well. PCS will be a less frequent diagnosis as patients are more efficiently screened and evaluated and as specific diagnoses are confirmed.
Follow-up care should be appropriate for the patient and the operation that was performed.
In a retrospective study of 105 patients, Coté et al investigated whether follow-up ERCP and bile duct balloon sweeps are necessary to find abnormalities in patients who have undergone endoscopic treatment for postcholecystectomy bile duct leakage.[19] Patients underwent initial ERCP at the time of bile leak treatment and follow-up ERCP after a mean interval of 6.9 weeks.
At follow-up, one or more abnormalities were found in 27.6% of patients, including persistent bile leak, CBD stones, and CBD sludge without stones.[19] Balloon sweeps, administered to a subgroup of patients, revealed a 17.6% prevalence of CBD stones or sludge at follow-up. In view of the prevalence of abnormalities after the endoscopic treatment of bile leaks, the authors recommended that follow-up ERCP and balloon sweeps be performed in patients at the time of stent removal.
The goals of pharmacotherapy are to reduce morbidity and prevent complications. Drug classes that may be considered in the medical management of patients with postcholecystectomy syndrome include bulking agents, gastrointestinal (GI) antispasmodic agents, bile acid sequestrants, histamine H2 antagonists, and proton pump inhibitors (PPIs).
Clinical Context:
Psyllium contains natural fiber that acts to increase the content of feces and, at the same time, promotes bacterial growth. The main indications for its use are in chronic constipation, irritable bowel syndrome, and bowel management in cases of patients with hemorrhoids.
Clinical Context:
Diphenoxylate is an antidiarrheal agent chemically related to the narcotic analgesic meperidine. It acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. It prolongs the movement of electrolytes and fluid through the bowel and increases viscosity and loss of fluids and electrolytes. A subtherapeutic dose of anticholinergic atropine sulfate is added to discourage overdosage, in which case diphenoxylate may clinically mimic the effects of codeine.
Clinical Context:
Cholestyramine may be used to treat diarrhea associated with excess bile acids. It binds bile acids, thus reducing damage to the intestinal mucosa. It also reduces the induction of colonic fluid secretion. It forms a nonabsorbable complex with bile acids in the intestine, which, in turn, inhibits enterohepatic reuptake of intestinal bile salts.
Clinical Context:
Colestipol forms a soluble complex after binding to bile acid, increasing fecal loss of bile acid–bound low-density lipoprotein cholesterol.
Clinical Context:
Nizatidine competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reductions in gastric acid secretion, gastric volume, and hydrogen concentrations.
Clinical Context:
Cimetidine inhibits histamine at the H2 receptors of gastric parietal cells, causing reductions in gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Clinical Context:
Ranitidine inhibits histamine stimulation of the H2 receptor in gastric parietal cells, reducing gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Like antacids, H2-receptor antagonists do not reduce the frequency of reflux but do decrease the amount of acid in the refluxate by inhibiting acid production. All H2-receptor antagonists are equipotent when used in equivalent doses. They are most effective in patients with nonerosive esophagitis. H2-receptor antagonists are considered the drugs of choice for children because pediatric doses are well established and the medications are available in liquid form.
Clinical Context:
Lansoprazole suppresses gastric acid secretion through specific inhibition of the H+/K+ -adenosine triphosphatase (ATPase) enzyme system (ie, proton pump) at the secretory surface of the gastric parietal cell. The drug blocks the final step of acid production, inhibiting basal and stimulated gastric acid secretion and therefore increasing gastric pH. Lansoprazole's effect is dose-related. The drug is easy to administer to children because it is available as a capsule or an oral disintegrating tablet or in granular form for use in an oral suspension.
Clinical Context:
Omeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATPase pump. It is used for both short-term treatment (4-8 weeks) and long-term treatment (up to 12 months) of gastroesophageal reflux disease.
Clinical Context:
Esomeprazole is an (S)-isomer of omeprazole. It inhibits gastric acid secretion by inhibiting the H+/K+ -ATPase enzyme system at the secretory surface of the gastric parietal cells. Esomeprazole is used in severe cases and in patients not responding to H2-antagonist therapy. The drug is administered for up to 4 weeks to treat and relieve the symptoms of active duodenal ulcers; it may be used for up to 8 weeks to treat all grades of erosive esophagitis.
Clinical Context:
Dexlansoprazole suppresses gastric acid secretion by specifically inhibiting the H+/K+ -ATPase enzyme system at the secretory surface of gastric parietal cells.
Clinical Context:
Rabeprazole sodium suppresses gastric acid secretion by specifically inhibiting the H+/K+ -ATPase enzyme system at the secretory surface of gastric parietal cells.
Clinical Context:
Pantoprazole suppresses gastric acid secretion by specifically inhibiting the H+/K+ -ATPase enzyme system at the secretory surface of gastric parietal cells.
PPIs are indicated in patients who require complete acid suppression (eg, infants with chronic respiratory disease or neurologic disabilities). They should be administered with the first meal of the day. Children with nasogastric or gastrostomy tubes may have granules mixed with an acidic juice or a suspension; tubes must then be flushed to prevent blockage.
What is postcholecystectomy syndrome (PCS)?What is the pathophysiology of postcholecystectomy syndrome (PCS)?What is the prevalence of postcholecystectomy syndrome and what are risk factors?Which patient groups are at highest risk for postcholecystectomy syndrome (PCS)?What is the prognosis of postcholecystectomy syndrome (PCS)?What are symptoms of postcholecystectomy syndrome (PCS)?What is included in the evaluation of suspected postcholecystectomy syndrome (PCS)?What is the role of lab studies in the workup of postcholecystectomy syndrome (PCS)?What is the role of radiography in the workup of postcholecystectomy syndrome (PCS)?What is the role of ultrasonography in the workup of postcholecystectomy syndrome (PCS)?What is the role of esophagogastroduodenoscopy (EGD) and colonoscopy in the workup of postcholecystectomy syndrome (PCS)?What is the role of endoscopic retrograde cholangiopancreatography (ERCP) in the workup of postcholecystectomy syndrome (PCS)?What is the role of CT scanning and MRI in the workup of postcholecystectomy syndrome (PCS)?What is the role of nuclear imaging in the workup of postcholecystectomy syndrome (PCS)?How are patients with postcholecystectomy syndrome (PCS) screened for coronary disease?What are the treatment options for postcholecystectomy syndrome (PCS)?When is pharmacologic therapy used to treat postcholecystectomy syndrome (PCS)?What is the role of surgery in the treatment of postcholecystectomy syndrome (PCS)?How is surgery performed for the treatment of postcholecystectomy syndrome (PCS)?How is postcholecystectomy syndrome (PCS) prevented?What is included in long-term monitoring of postcholecystectomy syndrome (PCS)?Which medications are used in the treatment of postcholecystectomy syndrome (PCS)?Which medications in the drug class Proton Pump Inhibitors are used in the treatment of Postcholecystectomy Syndrome?Which medications in the drug class Histamine H2 Antagonists are used in the treatment of Postcholecystectomy Syndrome?Which medications in the drug class Bile Acid Sequestrants are used in the treatment of Postcholecystectomy Syndrome?Which medications in the drug class Antispasmodic Agents, Gastrointestinal are used in the treatment of Postcholecystectomy Syndrome?Which medications in the drug class Bulking Agents are used in the treatment of Postcholecystectomy Syndrome?
Steen W Jensen, MD, Chief, Department of Surgery, Plumas District Hospital
Disclosure: Nothing to disclose.
Chief Editor
John Geibel, MD, MSc, DSc, 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; Fellow of the Royal Society of Medicine
Disclosure: Nothing to disclose.
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.
