- 1 What is Biliary Dyskinesia?
- 2 The Biliary System
- 3 Pathophysiology of Biliary Dyskinesia
- 4 Biliary Dyskinesia and its Risk Factors
- 5 Biliary Dyskinesia: Its Manifestations
- 6 How To Diagnose Biliary Dyskinesia
- 7 Treatment for Biliary Dyskinesia
- 8 Preventing Biliary Dyskinesia
What is Biliary Dyskinesia?
Dyskinesia literally means distortion or impairment of voluntary movements. Thus, biliary dyskinesia is defined as a motility disorder involving the Sphincter of Oddi and the gallbladder. It is an alteration in the normal movement of the Sphincter of Oddi, contraction of bile ducts and draining of the biliary tree. [1, 2, 3]
The Biliary System
To fully understand an abnormality, one should first know its normalcy. If biliary dyskinesia is an alteration of its movement, then what should its usual normal movement be like?
The biliary system is composed of the gallbladder, bile ducts and other structures implicated in the creation, transportation, storage and release of bile, a fluid which assists in the digestion and breakdown of fatty acids in the body. Its main tasks are to transport waste products from the liver to the duodenum, and to manage the release of bile for digestion. [4, 5]
Bile is secreted by the liver, gathered by the right and left hepatic ducts, and is drained into the common hepatic duct. This duct then eventually joins the cystic duct, forming the common bile duct. Only 50% of the bile traverse the common bile duct and set out to the duodenum. The other 50% accumulates in the gallbladder. 
Once stimulated by food, the gallbladder contracts, directing the bile towards the bile duct. During meal intervals, the gallbladder stores the bile, and upon eating, it contracts and empties itself. The said contraction is influenced by the hormone cholecystokinin and is assisted by the muscles of the Sphincter of Oddi. [6, 7]
An illustration of the biliary system, with bile travelling from the liver all the way to either the duodenum or the gallbladder.
Pathophysiology of Biliary Dyskinesia
There are a number of mechanisms by which the normal bile production and transportation process are altered. Below are the more common ones.
If the bile cannot be produced by the gallbladder, or if it cannot traverse the common bile duct, it will then reflux and go back in the gallbladder. This event will consequently lead to biliary dyskinesia. 
A nonfunctioning Sphincter of Oddi can also cause biliary dyskinesia. When the sphincter does not work correctly, bile cannot be transported through the common bile duct, and instead, will linger and accumulate in the bladder. Hence, biliary dyskinesia will ensue. [7, 8]
Biliary Dyskinesia and its Risk Factors
Alteration in bile transport and movement can be influenced by a number of factors. Presence of which may eventually result at increased risk for the disease. 
- Cholecystitis or inflammation of the bladder
- High levels of stress
- Low fat and low fiber diet
- Excessive use of antacids and medications for depression
- With history of inflammatory bowel disease
- Intake of too much sugar
- Previous history of thyroid dysfunction
- Low levels of gastric acid
- Increased alcohol intake
Biliary Dyskinesia: Its Manifestations
A prominent symptom of this illness is abdominal pain. This is localized in the right upper quadrant of the abdomen, but may also radiate to the upper back and the shoulder blades. It may occur 40-50 minutes after ingestion of foods high in fat. The pain may range from a vague dull aching discomfort, to a sharp stabbing pain. [6, 9]
Other symptoms brought about by indigestion of fats include bloating, burping, nausea, and vomiting. 
How To Diagnose Biliary Dyskinesia
Since biliary dyskinesia may have symptoms similar to cholelithiasis, the presence of gallstones must first be ruled out to come upon the diagnosis. Once the blood tests and ultrasound results reveal negative for lithiasis, further workup for dyskinesia shall be done. 
The diagnosis can be made with the use of CCK-HIDA scan, otherwise known as cholescintigraphy. This is a hepatobiliary iminodiacetic scan using cholecystokinin (CCK) to quantify the ejection fraction of bile coming from the gallbladder. A tracer marks the liver, gallbladder and the entire biliary system, allowing visualization of gallstones or sludges, if present. Ejection fraction will then be measured on a scale of 0 to 100%. Those of decreasing ejection fraction are prone to having inefficient gallbladder function, and hence are at risk for biliary dyskinesia. [10, 11, 12]
A photo showing a normal HIDA scan (A) and that with an abnormal finding (B).
Treatment for Biliary Dyskinesia
The most common treatment modality for biliary dyskinesia is laparascopic cholecystectomy, or surgical gallbladder removal. This can be done under general anesthesia, yet still on an outpatient basis. After the gallbladder has been removed, diminished abdominal pain may be experienced, with the digestion returning to its normal process. [6, 7, 8]
An illustration depicting a complete removal of the gallbladder done surgically via cholecystectomy.
A few herbal remedies may also be used as adjunct for the treatment of biliary dyskinesia. These can cause normal gallbladder movement and regulate hepatic secretion of bile. These include artichokes, yarrow, dandelion, and dandelion. 
The said adjuncts, however, are just supplements. Gallbladder removal, or cholecystectomy, still is the definitive treatment for biliary dyskinesia.
Preventing Biliary Dyskinesia
The following are steps by which biliary dyskinesia can be prevented 
- Avoid foods high in fat and oil
- Exercise and avoid a sedentary lifestyle
- Avoid stress, since it may also trigger biliary atresia
- Avoid frying foods, instead one may opt to boil or bake them
- Regular consult with physician, along with regular determination of cholesterol levels should be done, along with compliance in taking maintenance medications
- Toouli, J. Biliary Dyskinesia. Current Treatment Options on Gastroenterology. 2002 Aug; 5(4): 285-291
- Canfield, AF, et al. Biliary Dyskinesia: A Study of More Than 200 Patients and Review of the Literature. Journal of Gastrointestinal Surgery. 1998 Sept to October; 2(5): 443-8.