الفهرس 
Embryology of Biliary TractOnly 14 pages are availabe for public view
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Abstract
Dysfunction of the gall bladder and/or SO produces similar patterns of biliopancreatic pain and SO dysfunction may occur in the presence of the gall bladder. The symptom-based diagnostic criteria of gall bladder and SO dysfunction are episodes of severe steady pain located in the epigastrium and right upper abdominal quadrant which last at least 30 minutes. Gall bladder and SO dysfunctions can cause significant clinical symptoms but do not explain many instances of biliopancreatic type of pain. The syndrome of functional abdominal pain should be differentiated from gall bladder and SO dysfunction.
In the diagnostic workup, invasive investigations should be performed only in the presence of compelling clinical evidence and after non-invasive testing has yielded negative findings. Gall bladder dysfunction is suspected when laboratory, ultrasonographic, and microscopic bile examination have excluded the presence of gallstones and other structural abnormalities. The finding of decreased gall bladder emptying at cholecystokinin-cholescintigraphy is the only objective characteristic of gall bladder dysfunction. The diagnosis is made by performing a gallbladder ejection fraction, which is a radionuclide investigation. An abnormal gallbladder ejection fraction has a value less than 35%. Patients with an abnormal gallbladder ejection fraction should undergo cholecystectomy. This procedure has been shown to be effective in curing the symptoms in over 90% of patients. Symptomatic manifestation of SO dysfunction may be accompanied by features of biliary obstruction (biliary-type SO dysfunction) or significant elevation of pancreatic enzymes and pancreatitis (pancreatic-type SO dysfunction). Biliary-type SO dysfunction occurs more frequently in postcholecystectomy patients who are categorized into three types. Types I and II, but not type III, have biochemical and cholangiographic features of biliary obstruction. When non-invasive investigations and endoscopic retrograde cholangiopanreatography show no structural abnormality, manometry of both biliary and pancreatic sphincter may be considered. On manometry, diagnosis of a sphincter of Oddi stenosis should lead to division of the sphincter.
Sphincterotomy results in long-term relief of symptoms in more than 80% of patients. Also When sphincter of Oddi manometry of the pancreatic duct sphincter performed and manometric stenosis is diagnosed, these patients should undergo division of both the biliary and pancreatic duct sphincter. The division ensures that both the biliary and the pancreatic sphincters are divided to allow free drainage of pancreatic juice and bile into the duodenum. This treatment is recommended only in patients who have been shown by endoscopic manometry to have abnormal SO dysfunction as demonstrated by an elevated SO basal pressure in excess of 40 mm Hg. Traditionally, total division of the SO has been performed by an open transduodenal approach to the SO. Nowadays, the treatment of choice for pancreatic SO dysfunction is the endoscopic division of the pancreatic sphincter. Similar to the surgical approach, these patients undergo division of the biliary sphincter and subsequently division of the septum between the biliary and pancreatic ducts using diathermy techniques. This treatment results in relief of symptoms in more than 80% of patients.
Botulinum toxin acts by inhibiting presynaptic release of acetylcholine to inhibit contraction in smooth and striated muscle. The injection of Btx-A in Vater’s papilla is useful from a diagnostic and therapeutic viewpoint. As the tonus of Oddi’s sphincter is influenced by cholinergic innervation, endoscopic injection of Btx (20–100 U) produces a 50% reduction in the basal tonus according to various reports. This effect results in the long-term relief of biliary symptoms and allows the identification of subjects who will benefit from definitive sphincter ablation, avoiding the specific risks of endoscopic manometry. Moreover, the symptomatic response to Btx-A injection, which can last for a period of 6 weeks to 6 months, may suggest a therapeutic role of the toxin in the management of acute episodes.