Acute Chole Paper

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Michelle Blouin Acute Cholecystitis Etiology and Genetic Factors Acute Cholecystitis (ACC) is an acute inflammatory disease of the gallbladder, which is caused by gallstones in 90% - 95% of the cases (Kimura et al., 2007). According to Fromm and Mulagha (1999) interference with gallbladder emptying is caused by inflammation. Ischemia, motility disorders, direct chemical injury, infections with microorganisms, collagen disease and allergic reactions are just some of the causes of inflammation and obstruction of the gallbladder (Kimura et al., 2007). When gallstones are present, the degree of inflammation depends on the amount of obstruction and the length of time of the obstruction. According to Bellows and Berger (2005), strong risk factors for symptomatic gallstone disease are, a family history of a cholecystectomy, in a first-degree relative, and obesity (defined as body mass index greater than 30 kg per m2. Kimura et al. (2007), states that another risk factor for ACC, in obese individuals, is dieting or the drastic flunctuations of weight. It is well documented that the incidence of acute cholecystitis is higher in females than males, with a female to male ratio of 3:1 (Fromm and Mulagha, 1999). According to Kimura et al. (2007) levels of estrogen and progesterone are involvded in the formations of gallstones; therefore, women taking oral contraceptives or pregnant women are at greater risk of developing gallstones. Kimura et al. (2007) further discusses risk factors termed the termed “4F” or “5F” (fair, fat, female, fertile, and forty), with progesterone and estrogen levels being the common factor.

Pathophysiology With ACC, gallbladder neck distention and gallbladder wall edema, that can progress to venous lymphatic obstruction, ischemia, and necrosis, is caused by gallbladder neck obstructtion that causees an increase in intraluminal pressure (Barkun & Yusoff, 2003). Mediators that have been identified in the pathophysiology of ACC are cholesterol-supersaturated bile, lysolecithin, phospholipase A, and prostaglandins (Barkun & Yusoff, 2003). Prostaglandins are believed to play a key role in mediating inflammation (Barkun and Yusoff, 2003). If the obstruction is partial and of short duration the patient experiences biliary colic; however, if the obstruction is complete and of long duration the patient develops acute cholecystitis (Kimura et al, 2007). Fromm and Mulagha (1999) mentioned that the bile is often sterile initially, but bacterial infection may develop leading to a more serious disease pathology. The organisms most commonly cultured are enteric bacteria including Escherichia coli (E. Coli), Klebsiella, and Enterococcus (Burkun &Yusoff, 2003). Once a patient is symptomatic, the rate of biliary complications rises and prompt treatment is necessary to prevent serious complications. Clinical Manifestations/Physical Assessment The hallmark signs of ACC are acute onset of right upper quadrant (RUQ) pain (usually radiating to the shoulder blade), nausea, vomiting, and fever (Fromm and Mulagha, 1999). Another sign of ACC ,which is explained an an interruption of inspiration during deep palpation under the liver, is termed Murphy’s sign, and is a direct clinical finding, but not necessarily a constant one (Fromm & Mulagha, 1999). According to Barkun and Yusoff (2003), a positive Murphy’s sign is highly sensitive and predictive of ACC. Bellow and Berger (2005) emphasize that recurrent pain is common once symtpoms begin and serious complications are more likely to develop at this point.

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Laboratory and Diagnostic Assessment The combination of prolonged, constant right upper quadrant pain and tenderness with fever are highly suggestive of ACC (Barkun & Yusoff, 2003). For accurate diagnosis, labs should also be obtained and leukocytosis with increased neutrophils and band forms is usually present (Barkun & Yusoff, 2003). A definitive diagnosis is usually made with an ultrasound. Ultrasonagraphy does not always confirm the diagnosis of ACC, but is highly sensitive and specific for the presence of gallstones greater than 2mm (Barkun & Yusoff, 2003). Walling (2005) concurs and further reports that ultrasound can visualize the stones, measure the gall bladder wall thickness, and gallbladder distention commonly used to make the diagnosis of ACC. According to Fromm and Mulagha (1999), no test by itself is diagnostic; however, ultrasound is less expensive and easier to obtain. Recent research has shown that ultrasound is the diagnostic test chosen by physicians because it is non invasive, cost effective, involves no ionizing radiation, and has a reported specificity of 99 percent for detecting gallstones (Bellow & Berger, 2005). Conclusion If not treated promptly, Acute Cholecystitis can potentially be a serious pathological disease process leading to rupture, sepsis, and death. When a definitive diagnosis is made, surgical cholecystectomy has been the treatment of choice for ACC (Barkun & Yusoff, 2003). Cholecystectomy provides 92 percent of patients with complete relief of biliary pain, is safe and has the lowest patient risks (Bellows & Berger, 2005).

References Barkun, J.S. & Yusoff, I.F. (2003). Diagnosis and management of cholecystitis and cholangitis. Gastroenterology Clinics of North America. 32, 146-168. Doi:10.1016/S08898553(03)00090-6 Bellows, C.F. & Berger, D.H. (2005). Management of gallstones. American Family Physician, 72(4), 637-641. Retrieved from http://www.aafp.org/afp. Fromm, H. & Mulagha, E. (1999). Acute cholecystitis. Current Treatment Options in Gastroenterology. 2, 144-146. Kimura, Y., Takada, T., Kawarda, Y., Nimura, Y., Hirata, K., Sekimoto, M.,…Gadacz, T.R. (2007). Definitions, path physiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines. Journal of HBP Surgery. 14, 15-26. Doi:10.1007/s00534-006-1152-y. Walling, A.D. (2005). How well does ultrasonagraphy diagnose cholecystitis. American Family Physician. Retrieved from http://www.aafp.org/afp.