Differential diagnosis
(a) Retained bile duct stone
(b) Recurrent bile duct stone
(c) Remnant gallbladder
(d) Remnant duct cystic
(e) Bile duct injury (leak, ligature, or stricture)
(f) Spillage of stones
(g) Papillary stenosis
(h) Sphincter of Oddi dysfunction
(i) Pancreatic disease
(j) Acid-related disorders
(k) Hepatocellular disorders
(l) Functional dyspepsia
(m) Ischemic heart disease
(n) Musculoskeletal disorders
(o) Irritable bowel syndrome
Clinical manifestation of PCS may occur early in the postoperative period, usually because of incomplete surgery (e.g., retained calculi in the cystic duct remnant or in the common bile duct) or operative complications (e.g., bile duct ligature or bile leakage). A later onset is commonly caused by inflammatory scarring, strictures involving the sphincter of Oddi or the common bile duct, recurrent calculi, or spillage of stones into the abdomen. Symptoms of SOD may happen any time after cholecystectomy, and because it is not associated with any structural abnormalities, the approach to patients with suspected SOD often requires more attention.
SOD is a benign acalculous obstruction to the flow of biliary secretions through the sphincter of Oddi (SO). The cause of SOD remains speculative, but it could be associated with hormonal or neurological disturbances of the SO, leading to its intermittent obstruction despite the absence of organic abnormalities. Sphincter of Oddi dyskinesia refers to a primary motor abnormality of the SO, which may result in a hypotonic or, more commonly, a hypertonic sphincter. In contrast, SO stenosis refers to a structural alteration of the sphincter, probably from an inflammatory process with subsequent fibrosis. Because it is often impossible to distinguish patients with SO dyskinesia from those with SO stenosis, the term SOD has been used to incorporate both groups. Importantly, SOD can involve abnormalities in the biliary sphincter, pancreatic sphincter, or both. Non-biliary causes of PCS should always be investigated simultaneously.
Epidemiology
Postcholecystectomy syndrome occurs in 10–40 % of patients. The time to the onset of symptoms can range from days to years depending on the cause. Women may be at higher risk, with symptoms recurring in 43 % compared to 28 % in men. In about 5 % of patients who undergo laparoscopic cholecystectomy, the reason for chronic abdominal pain remains unknown. Among all possible causes of PCS, retained calculi in the common bile duct or cystic duct remnant are the most frequent.
As a functional disorder, SOD may coexist with other functional GI disorders such as gallbladder dyskinesia (i.e., functional gallbladder disorder), functional dyspepsia, gastroparesis, and irritable bowel syndrome. The estimated prevalence of SOD in the general population is 1.5 %, affecting women more frequently than men (3:1) and usually occurring between the ages of 20 and 50 years. SOD results in work absenteeism, disability, and significant healthcare utilization. Though it may occur in patients with gallbladder in situ, SOD is most commonly considered in patients who have previously undergone cholecystectomy.
The primary symptom of the SOD is pain. Although pain is considered a subjective complaint, substantial information can be obtained after careful questioning in determining whether the pain is biliary-like. Completely defining the pain features is essential. Data about location, intensity, frequency, duration, and other symptom associations should be collected. The classic location of pain is right upper quadrant and/or epigastric. Pain often radiates to the back, particularly the right shoulder, and classically begins 1–2 h after ingestion of a fatty meal; however, the relationship to food intake is considered unreliable. Many patients report pain occurring at night with a peak occurrence around midnight. While pain is recurrent, it recurs at variable intervals (not daily) and may be associated with nausea and vomiting. The pain typically plateaus in less than an hour and is severe enough to interrupt daily activities or require consultation with a physician. Once it has reached its peak, the pain usually lasts at least 30 min and then slowly subsides over several hours, with the entire attack usually lasting less than 4–6 h. These pain characteristics have been codified in consensus guidelines of a Rome III committee in order to standardize the qualities associated with biliary-type pain and to help diagnose functional gallbladder disorder and SOD (see Table 14.2). It should be emphasized that continuous, daily abdominal pain is not consistent with SOD.
Table 14.2
Functional gallbladder and sphincter of Oddi disorders diagnostic criteria (Rome III)
Functional gallbladder and sphincter of Oddi disorders diagnostic criteria must include episodes of pain located in the epigastrium and/or right upper quadrant and all of the following: |
---|
(a) Episodes lasting 30 min or longer |
(b) Recurrent symptoms occurring at different intervals (not daily) |
(c) The pain builds up to a steady level |
(d) The pain is moderate to severe enough to interrupt the patient’s daily activities or lead to an emergency department visit |
(e) The pain is not relieved by bowel movements |
(f) The pain is not relieved by postural change |
(g) The pain is not relieved by antacids |
(h) Exclusion of other structural disease that would explain the symptoms |
Supportive criteria: The pain may present with one or more of the following: associated with nausea and vomiting, radiates to the back and/or right infra-subscapular region, awakens from sleep in the middle of the night |
Pathophysiology
Choledocholithiasis after cholecystectomy may result from either a migrated gallbladder stone not detected in the perioperative period or a stone forming de novo in the common bile duct (secondary calculus), which develops as a result of biliary stasis often associated with strictures or papillary stenosis. When the symptoms of pain develop early, the possibility of bile duct stone should be investigated, even in the absence of jaundice or bile duct dilatation. Choledocholithiasis may be complicated by acute pancreatitis and cholangitis.
The mechanism by which the cystic duct stump is associated with PCS has been investigated. In one study of seven cases, retained gallbladder calculi and cystic duct remnant stones were found to be the cause of recurrent biliary symptoms. Some authors believe a long stump alone is not the cause of recurrent symptoms and the possibility of a remnant gallbladder must be kept in mind. The presence of a gallbladder remnant after cholecystectomy is very rare. The gallbladder remnant becomes symptomatic due to chronic inflammation or harboring gallstones. Other authors have suggested that PCS may arise from the cystic duct remnant or a neuroma of the cystic duct stump. In one series of three patients, pain was exacerbated during EUS with the patient lightly sedated by pushing on cystic duct surgical clips with an EUS-guided needle. The pain was temporarily alleviated by EUS-guided injection of bupivacaine and triamcinolone. In two patients, surgical resection of the cystic duct remnant was performed. Another consideration is neurogenic pain at the site of cholecystectomy, particularly open cholecystectomy. This entity may be managed by pain specialists with local injection therapies.
Factors that have been associated with bile duct injury include surgeon experience, patient age, male sex, and acute cholecystitis. Bile duct injury may result in a leak, stricture, or bile duct disruption. The main causes of ductal injury are erroneous cutting of bile ducts, inadvertently placed clips or ligatures, periductal bile leakage resulting in fibrosis, and thermal injury owing to electrocautery.
Spillage of stones into the abdomen can occur during dissection of the gallbladder off the liver bed, tearing with grasping forceps, or during extraction of the gallbladder through one of the port sites. It may result in intra-abdominal abscess, subcutaneous abscess, and later discharge of stones through the abdominal wall or biliary tract. The abscess may be diagnosed as “simple” when the stones are radiolucent.
The role of dysfunction at the level of the sphincter of Oddi in patients with presumed functional gallbladder disorder remains unclear. Although similar gallbladder ejection fractions in patients with and without documented SOD have been described, other reports describe a similar frequency of SOD in patients with and without gallbladder dysfunction based on gallbladder ejection fraction. In a prospective study designed to evaluate the relationship between SOD and gallbladder dysfunction, 81 patients with biliary-type pain and an intact, sonographically normal gallbladder underwent both SO manometry and cholecystokinin-HIDA cholescintigraphy. In 41 patients with a normal gallbladder ejection fraction, 57 % had SOD, while 50 % had SOD in the 40 patients with an abnormal gallbladder ejection fraction suggesting that both SOD and functional gallbladder dysfunction are common in this group of patients and appear to occur independently of one another.
For patients without a gallbladder suspected to have SOD, a biliary classification system was initially developed (Hogan–Geenen SOD classification system) based on clinical history, laboratory tests, and endoscopic retrograde cholangiopancreatography (ERCP) bile duct drainage times. Subsequently, the classification was modified by removing the biliary drainage times given practical limitations in determining drainage times and evidence suggesting that drainage times do not correlate with findings on SO manometry. The current classification contains three categories (see Table 14.3). Type I SOD consists of the presence of typical biliary pain, abnormal aminotransferase levels > 2 times the upper limits of normal on more than two occasions, and a dilated common bile duct (>10 mm) on noninvasive imaging. Type II SOD comprises biliary pain plus one of the other two additional criteria, elevated liver tests or common bile duct dilation but not both. Finally, type III SOD consists of biliary pain only with no objective criteria.
Table 14.3
Hogan–Geenen sphincter of Oddi dysfunction modified classification system
Typical pain | LFT > 2× normal | Bile duct > 10 mm | ||
---|---|---|---|---|
Type I | + | + | + | |
Type II | + | + | Or | + |
Type III | + | − | − |
Diagnosis and Evaluation
The diagnosis of PCS will depend on the patient’s history, clinical symptoms, and laboratory and imaging exams. Biliary and non-biliary causes need to be considered. For instance, biliary duct injury may lead to bile leakage, intra-abdominal abscess, cholangitis, and secondary biliary cirrhosis due to chronic strictures. Early postcholecystectomy symptoms such as fever, abdominal pain, and jaundice may be associated with retained stones or bile duct injury (leak or ligature). The same symptoms 2 years after cholecystectomy may be secondary to recurrent stones or bile duct stricture. Patients with a gallbladder remnant complain primarily of pain and rarely develop jaundice. Papillary stenosis usually presents with biliary-type abdominal pain, significantly elevated liver enzymes, and a dilated common bile duct without evidence of stones. The symptoms of papillary stenosis more commonly have a later presentation. Retained or recurrent stones and bile duct injury may be complicated by acute cholangitis. SOD may be present prior to cholecystectomy or any time after cholecystectomy.
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