Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Biliary dyskinesia and sphincter of Oddi dysfunction (SOD) are functional disorders of the pancreas and biliary tract that challenge the practicing surgeon. Both disease entities are characterized by pancreatobiliary pain syndromes and are fraught with controversy over their definition, diagnosis, and management. In addition, both disorders have been the subject of recent important study, potentially affecting management.
Acalculous gallbladder disease has been recognized by surgeons for almost a century. In 1924 Alfred Blalock described a series of greater than 100 patients who underwent cholecystectomy in the absence of gallstones with excellent results in pain relief (83% were improved). In 1926 Allen Oldfather Whipple reported on 36 of 47 patients (76%) who were improved with cholecystectomy for acalculous biliary disease.
Biliary dyskinesia is a disease process characterized by right upper quadrant biliary-type pain in the absence of gallstones. Biliary dyskinesia is also referred to as chronic acalculous cholecystitis , acalculous biliary pain, and functional gallbladder disorder . Biliary dyskinesia is presumed to represent pain secondary to the abnormal motile function of the gallbladder. The frequency of acalculous biliary pain may be as high as 8% in men and 21% in women.
The purpose of the gallbladder is to store and concentrate bile after production by the liver. Gallbladder emptying is achieved by contraction of the smooth muscle of the gallbladder wall, which occurs in coordination with sphincter of Oddi relaxation. In the fasting state the gallbladder empties partially cyclically in conjunction with the migrating motor complex. In response to meal intake, contraction of the gallbladder occurs because of neural reflex stimuli, as well as enterohormonal cues from the foregut, most notably cholecystokinin (CCK).
The pathophysiology of biliary dyskinesia is incompletely understood. In some cases the cystic duct is implicated as problematic, with narrowing, possibly because of inflammation or fibrosis, and a resultant obstruction to gallbladder emptying. In other cases an intrinsic functional motility disorder of the smooth muscle of the gallbladder wall or the cystic duct seems to be causative. Biliary dyskinesia has been associated with other gastrointestinal motility disorders, including irritable bowel syndrome, colonic inertia, and gastroparesis. Alterations in bile composition, as well as inflammatory mediators (prostaglandin E 2 ), have also been implicated in biliary dyskinesia. Interestingly, up to 43% of gallbladders on final pathology after cholecystectomy for presumed biliary dyskinesia show no histologic abnormalities.
Likely, biliary dyskinesia encompasses a diverse group of patients with variable factors contributing to poor gallbladder emptying.
Patients with biliary dyskinesia present with typical pancreatobiliary-type pain, as outlined by the Rome IV diagnostic criteria, in the absence of gallstones ( Box 110.1 ). The pain is located in the right upper quadrant or epigastrium, is colicky in nature, occurs postprandially, and is typically associated with nausea or bloating. The patient may have associated emesis or diarrhea. In addition, the patient may report anorexia and weight loss.
Pain located in the epigastrium and/or right upper quadrant and all of the following:
Builds up to steady level and lasting 30 minutes or longer
Occurring at different intervals (not daily)
Severe enough to interrupt daily activities or lead to an emergency room visit
Not significantly (<20%) related to bowel movements
Not significantly (<20%) relieved by postural change or acid suppression
The pain may be associated with:
Nausea and vomiting
Radiation to the back and/or right infrascapular region
Waking from sleep
Biliary pain
Absence of gallstones or other structural pathology
Low ejection fraction on gallbladder scintigraphy
Normal liver enzymes, conjugated bilirubin, amylase/lipase
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here