Acute Cholecystitis Case Study Analysis

Introduction

The biliary system consists of the gall bladder, bile ducts and associated system that are involved in the secretion and transportation of bile. The biliary system’s main functions are to drain waste products from the liver into the duodenum and controlled release of bile to aid in digestion.  The greenish-yellow bile is produced by liver cells and consists of cholesterol, bile salts and some waste products. Bile salts, particularly, help in digestion of fats and remove waste. Bile is then excreted out of the body in faeces (Keus et al 2006). A complication of gallbladder, Cholecystitis may be classified as acute or chronic. In acute cholecystitis (AC) the gall bladder is dilated and is edematous. Its wall is thickened and inflamed (Lack 2003). Acute acalculous cholecystitis seems to progress more rapidly to gangrene and perforation than acute calculous cholecystitis (gallstones induced cholecystitis). Thus a timely diagnosis involving combination of clinical signs, laboratory findings and imaging techniques is necessary. (Keus, Broeders, and Laarhoven 2006).

Since the symptoms of cholecystitis resemble other medical complications and at times typical signs of AC may be poorly distinguished in some scans as in Computed tomography (CT) which is not sensitive or specific for AC and is, therefore, an accurate diagnostic process with high specificity is required. The article discusses role of various imaging modalities in identification of AC cases.

 Aetiology:

Cholecystitis is an inflammation of the gallbladder wall and nearby abdominal lining. It is usually caused by a gallstone in the cystic duct, the duct that connects the gallbladder to the hepatic duct (calculous AC). Other causes of cholecystitis may include the bacterial infection in the bile duct system, tumor of the pancreas or liver , decreased blood supply to the gallbladder (Acalculous AC). Pregnant women may develop cholecystitis due to accumulation of thick layer of gallbladder sludge.  It is made up of fine particles of material similar to gallstone. Kimura et al (2007) state that Acute cholecystitis also has other causes, besides the gallstones, such as ischemia; certain hemicals that enter biliary secretions; drug disorders; infections with microorganisms, protozoa, and parasites; collagen disease; and allergic reactions. Acute acalculous cholecystitis is also associated with a recent operation, trauma, burns, multisystem organ failure, and parenteral nutrition

 Epidemiology:

About 10% of population has gallstones.  In the younger age group the incidence of gallstones in female to male has ratio of 2:1 which increases in females with advancing age. After 60 years of age 10-15% males have gallstones compared to 20-40% females. The prevalence of gallstones in females is also associated with childbearing, HRT, oral contraceptives and obesity. Majority of cases are calculous cholecystitis while acalculous cholecystitis is caused to 5-15% cases only (Lack 2003).

The mortality is reported less than 10% for AC giving impression that it is not a fatal disease, except for the elderly and/or patients with acalculous disease (Kimura et al 2007). Sharma and Steel (2009) referred literature regarding mortality and morbidity due to AC cholecystitis. Gallstones result in morbidity when these become symptomatic. The incidence of AC is falling mostly due to increased acceptance by patients of laparoscopic cholecystectomy (removal of gall bladder) as a treatment for symptomatic gallstones. However immunocompromised patients may show mortality of up to 15%.  Complicated cholecystitis has 25% mortality (eg, gangrene, emphysema of gallbladder). Perforation of gallbladder occurs in 3-15% of patients with cholecystitis and is associated with 60% mortality. People of Hispanic or northern European countries are more likely to have gallstones.

 A brief case history:

A 51-year old woman presented to the emergency room with a 24-hour history of abdominal pain that began approximately one hour after a reportedly heavy party dinner. The pain began as a dull ache in the epigastrium but then localised in the right upper quadrant (RUQ). She reports some nausea but no vomiting. Since her arrival to the ER, the pain has decreased significantly. She also confirmed about a few such previous episodes in the recent past. Her medical history is significant for type II diabetes mellitus. On physical examination, her temperature is 38.0 C . Other vital signs are normal. The abdomen shows tenderness in the RUQ. The liver, rectal and pelvic examinations are normal. Her WBC count is 13,000/mm on arrival. Serum chemistry revealed total bilirubin 1.8 mg/dL, direct bilirubin 0.6 mg/dL, alkaline phosphatase 130 U/L, AST 50 U/L and ALT 35 U/L. Ultrasonography of the RUQ demonstrates stones in the gallbladder, a thickened gallbladder wall, and a common bile duct diameter of 4.0 mm (Tsai et al 2005).

Clinical Diagnosis:

Acute cholecystitis is defined as an inflamed gallbladder resulting in pain, especially in

the right hypochondrium, generally with accompanying fever and leucocytosis. Ultrasound may show thickening of the gallbladder wall and a hypoechogenic rim or halo (Keus et al 2006).  It is usually caused by a gallstone in the cystic duct. A typical attack of cholecystitis lasts two to three days. The major symptoms of cholecystitis may include: intense and sudden pain in the upper right quadrant of the abdomen, recurrent painful attacks for several hours after meals, pain that gets worse with deep breaths and may pass on to right shoulder blade, nausea, vomiting, abdominal bloating, chills, jaundice. The patients may experience these symptoms to different degree (Spira et al 2002). The diagnosis of acute cholecystitis was made in patient who presented with right upper quadrant or epigastric pain of more than 2 hours’ duration, had RUQ tenderness with localised peritoneal signs, and had a confirmatory radiologic study demonstrating gallstones as evidence of acute cholecystitis. Most frequently, patients had abdominal ultrasound studies that demonstrated gallstones as well as gallbladder wall thickening, pericholecystic fluid, and an ultrasound-induced Murphy’s sign (Madan et al 2002). The present case correlate well with the symptoms of acute cholecystitis as there are other indicators viz. lecucocytosis, enhanced levels of bilirubin, ALT, ASP and ALP and elevated temperature.  Diabetic patients are at a risk of decreased blood supply to gall bladder and are on controlled diet. The patient’s condition was probably aggravated on this account combined with heavy meal (likely to be high fat).

 Anatomy of Billiary System:

The normal gall bladder (GB) is A pear shaped sac attached to the under surface of right lobe of the liver (Fig 1). It is covered with a stretch of peritoneum to about 60% of its surface however the surface covered may vary.  The adult GB is about 10 cm in length and 3-4 cm in width. The wall is usually 1-2 cm thick but the wall thickness varies depending whether the gall bladder is relaxed or contracted.  The organ has three parts   broad outer part is  fundus, central body part and a ‘S’ shaped neck with infundibulum.  The neck connects GB with cystic duct. The mucosa of cystic duct is gathered into folds, near the neck forming spiral valves.  These valves contain smooth muscle fibres in the lumen controlling filling and emptying of gall bladder. The capacity of adult GB is 40 -70 ml though it can accommodate upto 100ml fluid.  Cystic duct is 2.5 cm in length and opens into dueodenum at other end.  The length of cystic duct appears smaller (1.5 cm) than its anatomic length due to tortuous path (Lack 2003)..

The GB concentrates,stores and release bile produced by liver cells. Besides, the organ secretes gall bladder mucins with role in protection of epithelium. The intake of fatty meal and, to some extent, proteins cause contraction of GB.  Cholecystokinin is the hormone responsible for contraction GB wall as a result emptying of bile into duodenum occurs (Lack 2003).

Pathology:

Acute cholecystitis causes sudden, severe pain in the upper right part of abdomen. The majority patients have gallstone and have inflamed gall bladder walls usually without infection which may set in afterwards. The fluid in the gall bladder walls cause these walls to thicken.  Acalculous cholecystitis is a rare occurrence and may be due to major surgery, critical illness or injuries including burns and sepsis. The long fasting or intravenous feeding may also cause acalculous cholecystitis.  This is more severe form of cholecystitis than calculous  (gallstone) cholecystitis and occurs in young children due to infections. Chronic cholecystitis is gallbladder inflammation that has lasted a long time and is always due to gallstones. It is characterized by repeated attacks of biliary colic (Yasutoshi et al 2007). The pathological examinations show leucocytosis, elevated levels of bilirubin and serum enzymes viz.Alkaline phosphatase, Alanine transaminase (ALT) and Aspartate transaminase (AST).

Role of Imaging Modalities in the Diagnosis of Acute Cholecystitis:

Imaging modalities in association with medical history and clinical examination help in diagnosis of acute cholecystitis.  Ultrasound or ultrasonography can also detect fluid around the gallbladder or thickening of its wall, which are typical of acute cholecystitis. Hepatobiliary scintigraphy is useful when acute cholecystitis is difficult to diagnose. In this test, If the radionuclide does not fill the gallbladder, the cystic duct is probably blocked by a gallstone. cholangiography is x-ray examination of the bile ducts using an intravenous (IV) dye. In percutaneous transhepatic cholangiography (PTC) a needle is introduced through the skin and into the liver where the dye (contrast) is deposited and the bile duct structures can be viewed by x-ray. Similarly, Endoscopic retrograde cholangiopancreatography (ERCP) examines the inside of these organs and detect any abnormalities.  Computed tomography scan (CT or CAT scan) is a diagnostic imaging procedure using a combination of x-rays and computer technology to produce cross-sectional images or slices in different planes, of the body (Cheng et al 2004). Rosen et al (2001) suggested choice of the sonographic Murphy’s sign, different from the clinical Murphy’s sign used during physical examination of gallbladder, to increase sensitivity of US to 91%. Physicians from the emergency department and admitting surgeons request both US and cholecystoscintigraphy (HIDA) for definitive diagnosis.  Kalimi et al (2001) found HIDA  to show 86% sensitivity while US was only 48% thus they suggested HIDA could be used alone to diagnose AC. Bingener et al(2004) also reported 60% accuracy of US for AC detection. While sonography is very sensitive for the detection of gallstones, the ability to predict acute cholecystitis in patients with clinical symptoms appears limited. The scans from different imaging techniques are shown in Fig 2-4 below. Loud et al (1996) believe that an advantage of the MR technique is that %CE is an independent and more accurate determinant of acute inflammation than wall thickness (Fig 5). However, the ability to elicit a positive Murphy’s sign is an advantage of sonography over MRI.

Treatment and Prognosis of Acute Cholecystitis:

 Specific treatment for cholecystitis is determined by the age, general health and medical history of the patient.  The treatment is also dependent on extent of the disease and patient’s Preferences and tolerance to medicine and procedures. Treatment for acute cholecystitis usually involves hospital stay to reduce stimulation to the gallbladder. Antibiotics are administered to reduce the inflammation and/or fight the infection. The treatment may also use drugs made from bile salts to dissolve stones. Low fat diet and pain management proves beneficial.  Sometimes, the gallbladder is surgically removed (cholecystoctomy) usually by laparoscopy (Paran et al 2006). Keus et al (2006) explain that aims of cholecystectomy in acute cholecystitis are threefold as: symptom relief, prevention of progression to complications, and prevention of recurrences of gallbladder disease. Cheng et al (2004) caution that high-density gallbladder wall sign is not only a specific sign for acute cholecystitis, but also a guarded predictor for acute gangrenous cholecystitis. If acute cholecystitis is confirmed and the risk of surgery is small, the gallbladder is usually removed within 24 to 48 hours after symptoms start. If necessary, surgery can be delayed for 6 weeks or more while the attack subsides. Delay is often necessary for people with a disorder that makes surgery too risky (such as a heart, lung, or kidney disorder). If a complication such as an abscess, gangrene, or perforated gallbladder is suspected, immediate surgery is necessary. In acute acalculous cholecystitis immediate removal of gall bladder is necessary (Paran et al 2006). The overall prognosis for cholecystitis is favorable. In some individuals, complications may arise if other organs are involved. Gallstones can return in the bile duct system after surgical removal of the gallbladder. Some patients experience pain even after removal of gall bladder (Paran et al 2006). It may be due to malfunction of sphinctor of Oddi that control flow of bile and pancreatic secretion. The other causes of pain like gall bladder attack may be small stones in the ducts, peptic ulcers or irritable bowel syndrome.

Summary and Conclusion:

The gall bladder inflammation is effectively diagnosed by combined clinical and radiologic examinations.  Although the imaging modalities are sensitive to diagnosis of AC, physicians normally request scans by more than one technique for enhanced accuracy.  The researchers differ in this regard.  They believe that a single technique that correlates well with clinical and histological examination is sufficient.  Some researchers also emphasise that modification of techniques to visualise exclusive signs of AC is desired (Kalimi et al; Cheng, Ng, and Shih 2004).  For example, signs such as gallbladder wall thickening, gallbladder distention and, pericholecystitic fluid are present in patient not having AC. A CT technique without contrast enhancement revealed hyperdense gall bladder wall as high probable sign of acute gangrenous cholecystitis.  Such patient should be given immediate treatment (Cheng et al 2004). The acceptance of laparoscopic cholestectomy has reduced complications due to AC.

References:

1. Bingener, J., W.H. Schwesinger, S. Chopra, M.L. Richards, and K.R. Shrinek. 2004.Does the correlation of acute cholecystitis on ultrasound and at surgery reflect a mirror image? The American Journal of Surgery. 188: 703-707.
2. Britannica (encyclopaedia). 2003. https://cache-media.britannica.com/eb-media/16/74316-004-386EA754.jpg [Accessed 22 Sep 2009] –
3. Cheng, She-Meng, Suk-Ping, Ng,and Shin-Lin, Shih. 2004. Hyperdense gallbladder wall sign: An overlooked sign of acute cholecystitis on unenhanced CT. Journal of Clinical Imaging, 28: 128-131.
4. van, Adriaan, Breda Vriesman, Robin Smithuis, Dries van Engelen, and Julien B.C.M. Puylaert . 2006. Gallbladder: Wall Thickening.  HYPERLINK “https://www.radiologyassistant.nl/en/43a0746accc5d” https://www.radiologyassistant.nl/en/43a0746accc5d (Accessed 27 sep 2009).
5. Kalimi, R., G.R. Geselter, D. Caplin, M. Brickman, G. T. Tronco, C. Love et al. 2001. Combined sonography-cholescintigraphy . J Am Coll Surg. 193(6): 609-613.
6. Keus, I. A. M. J., and Broeders, C. J. H. M. van Laarhoven. 2006. Surgical aspects of symptomatic cholecystolithiasis and acute cholecystitis.  Best Practice and l Research clinical gastroenterology, 20, 6: 1031-1051.
7. Lack, Earnest E. 2003. Pathology of pancreas, gallbladder, extrahepatic biliary tract and ampullary region. New York: Oxfors University Press, 2003.
8. Loud, P., R. C. Semelka, U. Kettritz, J. J. Brown, and C. Reinhold. 1996. MRI of acute cholecystitis: Comparison with the normal gall bladder and other entities. Magnetic Resonance Imaging. 14 (4): 349-355.
9. Madan, A. K.,S. Aliabadi-Wahle, D. Tesi, L. M. Flint, and S. M. Steinberg. 2002. How early is laparoscopictreatment of acute cholecyctitis. The American Journal of Surgery. 183:232-236.
10. Paran, Haim, Rivka Zissin, Eran Rosenberg, Igal Griton, Eugene Kots, and Mordechai Gutman. 2006. Prospective evaluation of patients with acute cholecystitis treated with percutaneous cholecystostomy and interval laparoscopic cholecystectomy. International Journal of Surgery 4 (2):101-105.
11. Tsai, Yuan-Ming, Chiao-Hsiung Chuang, Hsiu-Chi Cheng, Wei-Lun Chang, Ai-Wen Kao, and Chiung-Yu Chen. 2005. Usefulness of Fatty-meal Stimulated Gallbladder Contractility by Ultrasonography in the Diagnosis of Acute Cholecystitis. Journal of Medical Ultrasound 13 (4):179-185.
12. The Merck Manuals online Library. 2007. Cholecystitis. HYPERLINK “https://www.merck.com/mmhe/sec10/ch140/ch140c.html” https://www.merck.com/mmhe/sec10/ch140/ch140c.html (Accessed 1 Oct 2009).
13. Rosen, C. L., D. F. M. B rown, Y. Chang, C. Moore, N. J. Averill et al. 2001. Ultrasonography by emergency physicians in patients with suspected cholecystitis. American Journal of Emergency Medicine, 19 (1):.
14. Sharma, R, and Steel, P.A.D. 2009. Cholecystitis and Biliary Colic HYPERLINK “https://emedicine.medscape.com/article/774443-overview%20%20%20%5d28” https://emedicine.medscape.com/article/774443-overview (Accessed 29 Sep 2009).
15. Spira, Ram M., Aviran Nissan, Oded Zamir, Tzeela Cohen, Scott I. Fields, and Herbert R. Freund. 2002. Percutaneous transhepatic cholecystostomy and delayed laparoscopic cholecystectomy in critically ill patients with acute calculus cholecystitis. The American Journal of Surgery 183 (1):62-66.
16. Yasutoshi, K., T. Tadahiro, K. Yashifumi, N. Yuji, H. Koichi, and S. Miho et al. 2007. Definitions pathophysiology and epidemiology of acute cholangitis and cholecystitis. Journal Hepato-Billiary-Pancreatic Surgery. 14(1): 15-26.