Gallbladder Anatomy and Physiology
The gallbladder is responsible for the storage, concentration, and secretion of bile. Bile is a yellowish-green substance that is essential for the proper digestion of lipids. The gallbladder is part of the biliary tract of the gastrointestinal system and is located in the right upper abdominal quadrant, attached to the under surface of the liver at the gallbladder fossa. The gallbladder is connected to the biliary tract via the cystic duct. The gallbladder is a hollow, pear-shaped organ comprised of a fundus, body, and neck that measures approximately 7-10 cm long in adults. The wall of the gallbladder is comprised of multiple layers: the innermost layer is a mucosal layer made of epithelial cells, the muscularis layer is comprised of smooth muscle cells, and a membranous serosa surrounds the muscularis (Behar, 2013).
Figure 6. Gallbladder. (PDQ Adult Treatment Editorial Board, 2018).
Bile is synthesized by the liver and secreted into the common hepatic duct where it travels to the cystic duct and then to the gallbladder. The structure of the gallbladder wall allows for easy absorption of fluid and electrolytes (McCance, S. & Huether, S.E, 2019). Materials absorbed by the gallbladder wall are transported to the lymphatic system, leaving behind highly concentrated bile that is stored in the gallbladder until it is needed to emulsify ingested fats. Contraction of the muscularis layer of the gallbladder wall expels concentrated bile back into the cystic duct where it travels through the common bile duct to the ampulla Vater, and finally into the duodenum through the sphincter of Oddi (American Association of Medical Colleges and Khan Academy, 2019). The contraction of the muscularis is initially mediated by the parasympathetic fibers of the Vagus nerve during the cephalic and gastric phases of digestion. A hormone called cholecystokinin (CCK), however, is the primary mediator of muscularis contraction (McCance, S. & Huether, S.E, 2019). CCK is released by the small intestine when fats are present in the duodenum and jejunum (American Association of Medical Colleges and Khan Academy, 2019).
Cholecystitis: Pathophysiology and Clinical Manifestations
McCance, S. & Huether, S.E. (2019) define cholecystitis as inflammation of the gallbladder. Inflammation of the gallbladder can be caused by several different pathological conditions including obstruction in the biliary tract, infection, or neurological dysfunction that inhibits gallbladder emptying. Cholelithiasis is the most common cause of cholecystitis. The inflammation results in histologic changes to gallbladder cells ranging from mild swelling and edema to necrosis (Zakko, S. & Afdhal, N., 2018ba). Severe inflammation and obstruction can lead to perforation or rupture of the gallbladder.
The primary risk factor for the development of cholecystitis is the presence of cholelithiasis. Some risk factors for developing cholelithiasis are female gender, obesity, taking oral contraceptives, individuals over forty years of age, consuming a high-fat diet, and having a sedentary lifestyle (Zakko, S. & Afdhal, N., 2018b). Cholecystitis can be caused by other disease processes that interfere with gallbladder function such as cancer, infection, and vascular disease (Afdhal, N., 2019). Some studies suggest that genetic factors may play a role in the development of the condition as well (Mutar Mahdi, B., 2016).
According to McCance, S. & Huether, S.E. (2019), symptoms of cholecystitis are severe pain in the right upper abdominal quadrant that may radiate to the back or right shoulder, low-grade fever, and leukocytosis. Tachycardia can be present as a result of fever. Pain associated with cholecystitis is usually constant and severe. Rebound tenderness (pain that is experienced with the sudden release of abdominal pressure) is often present as well as a positive Murphy’s sign (pain that worsens during simultaneous palpation of the gallbladder and deep inspiration). Other symptoms may include nausea and vomiting or pain that worsens after eating, especially if the meal was large or high in fat content. Most laboratory values will remain normal in cholecystitis unless there is retrograde involvement of the liver or pancreas. According to Zakko, S. & Afdhal, N., elevations in inflammatory markers such as C-reactive protein may also be present (2018a).
G.B.’s clinical presentation is highly suspicious of cholecystitis. G.B. is female, obese, and reports a sedentary lifestyle. G.B. has severe, constant pain in her right upper quadrant that radiates to her back. She also reports nausea and a history of similar pain that worsens after eating and at night. G.B. has a low-grade fever and is mildly tachycardic. The examination of G.B.’s abdomen elicits a positive Murphy’s sign and rebound tenderness. G.B.’s laboratory testing reveals a slightly elevated white blood cell count, while her liver and pancreatic enzymes are normal. G.B.’s mother has a history of gallbladder disease.
Diagnosis and Treatment of Cholecystitis
G.B. will need imaging studies to finalize the diagnosis of her condition. Zakko, S. & Afdhal, N. (2018a) report that tests and procedures performed for the accurate diagnosis of cholecystitis include abdominal ultrasound or computerized tomography. Gallbladder edema or wall thickening greater than 4-5 mm supports the diagnosis of cholecystitis. If the diagnosis of cholecystitis cannot be confirmed following ultrasonography or CT, a hepatobiliary iminodiacetic acid (HIDA) scan using radioactive dye to track the flow of bile through the biliary tract is indicated.
Treatment for cholecystitis most generally involves hospitalization, fasting to minimize stress on the gastrointestinal system, intravenous fluids, antibiotics, and pain control. An endoscopic retrograde cholangiopancreatography (ERCP) may be required to relieve cystic duct occlusion and cholecystectomy may be required in severe cases or for complications such as perforation or rupture (McCance, S. & Huether, S.E., 2019).
Figure 7. Ultrasound Image. (Gibson, C.M. & Furqan, M.M. (Eds.), 2018).