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Ascending Cholangitis and Acute Cholecystitis Cases - Case Study Example

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The paper "Ascending Cholangitis and Acute Cholecystitis Cases" describes that the main symptom is a pain in the RUQ of the abdomen. Other symptoms related to AC include nausea and vomiting. On physical examination, the abdomen is very tender to touch…
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Topic: Acute Cholecystitis Name: Student Registration No. Institution name: Tutor’s name: Due date: Table of Contents 2.Case Study 3 3. Anatomy of the Biliary System 4 3.Pathology (aetiology, risk factors, pathogenesis) 5 Introduction The main emergencies of biliary tract include acute pancreatitis, ascending cholangitis, and Acute Cholecystitis1. These conditions normally come about because of calculi obstruction to the gallbladder or the biliary tree. Less commonly they may arise from malignant or benign strictures of the biliary sludge, biliary tree manipulation, or biliary tree. Regardless of the advances in the therapy, conditions like these cause significant mortality and morbidity, specifically among the elderly2. This is a case study paper on Acute Cholecystitis that covers the anatomy, pathology, clinical presentation, role of imaging modalities in the diagnosis, and treatment. 1. 2. Case Study A 68 year old woman presented to the emergency department with nausea, postprandial Right Upper Quadrant (RUQ) pain, and emesis for the past twelve hours. The pain is persistent and radiates to the back. She is afebrile. On palpation in the RUQ, her abdomen is tender. Sonography indicates cholelithiasis (presence of gallstones) as demonstrated in figure 2, ultrasound showed thickening of the gallbladder as indicated in Figure 3, and an enlarged common bile duct which measures 12mm. Laboratory findings showed the following: AST 222U/L, alkaline phophatase 385 U/L, WBC 13,000/mm, and direct bilirubin 4.0mg/dL. The patient is diagnosed for Acute Cholecystitis as indicated in figure 4. 3. Anatomy of the Biliary System The biliary system entails the ducts and organs (gallbladder, bile ducts, and related structures) (Figure 1) that are engaged in the generation as well as transportation of bile (Portincasa et al 2006). The gallbladder is the sac that holds bile3. It has three layers which are serous (outer), fibrous/muscular and mucousal which is the inner layer. The gallbladder has three components which include the fundus, body and the neck 4. The gallbladder is situated on the liver’s inferior surface and it is 7-10 cm long5. The biliary system consists of the ducts as well. The hepatic ducts are responsible for bile’s drainage from the liver to the gallbladder or directly to small intestines. There is the right, left and the common hepatic ducts. The cystic duct is 3 to 4 cm long. It extends from the gallbladder and connects with the common hepatic duct to create the common bile duct. The cystic duct has a spiral valve. The common bile duct is formed through the cystic duct and common hepatic duct’s junction and expands down to the hepato-pancreatic ampule. Hepatopancreatic ampule is formed by the main pancreatic duct and the common bile ducts’ junction. It ends with the hepatopancreatic sphincter. It drains into the duodenum via the duodenal papilla6. Abnormal finding in this anatomy with regards to the case study is that there is thickened gallbladder and enlarged common bile duct. Figure 1. Biliary System Anatomy (From Van De Graaff et al 2010) 3. Pathology (aetiology, risk factors, pathogenesis) Acute cholecystitis (AC) refers to the gallbladder’s acute inflammation7. Gallstones present in more than 90 percent of cases, and bring about constant obstruction of the outlet of the gallbladder due to the impaction within the gallbladder’s neck, cystic duct, or Hartmann’s pouch8. Gallstones are omnipresent; however, since several patients are actually asymptomatic, there is uncertainty in their exact incidence9. Other factors involved in acute cholecystitis include collagen disease; infections with protozoa, microorganisms, and parasites; allergic reaction; direct chemical injury; motility disorders; and ischemia (Yasutoshi et al 2007). There are various risk factors associated with AC10. AC is the leading complication that occurs in patients who have cholelithiasis. One of the risk factors is AIDS. Abnormal liver functions and/or enlarged liver are seen in 2/3 of patients with AIDS, a number of whom have diseases of the biliary tract11. In AIDS patients, biliary disease might take place through two mechanisms: through AIDS Cholangipathy (most frequent) and through acute Acalculous Cholecystitis. Another risk factor is drugs. Among several drugs in management of hyperlipidemia, fibrate is indicated to have an association with gallstone illnesses. There is a report stating that octreotide long-term administration brings about cholestasis, and that its one year administration brings about cholelithiasis in 50 percent of patients, particularly in level 4. Infusion of hepatic artery will bring about chemical cholecystitis. Ampicillin and Erythromycin are shown to cause hypersensitive Cholecystitis12. Ascaris have also been linked to Acute Cholecystitis. With regards to AC’s pathogenesis, various factors add to AC’s development: obstruction of the bile duct, biliary sludge, bacteria, supersaturated bile, biliary crystals, and vascular compromise13. Cystic duct obstruction is considered as most significant, resulting in distension and a rise in intraluminal pressure. The consequential disruption to the epithelium’s normal mechanisms of defense results in the gallbladder’s exposure to bacteria. The vascular compromise, particularly in patients who are critically ill and are subjected to hypotension episodes, is thought to be another causative factor 14.Ischaemia, reperfusion injury, and decreased blood flow cause damage to the gallbladder and reduce its natural resistance of anti-inflammation. 4. Role of Imaging Modalities in the Diagnosis of Acute Cholecystitis AC is a frequent Epigastralgia’scause where sonogram normally acts as the initial imaging modality because of its gallstone detection’s high sensitivity15. In terms of the potential to demonstrate Murphy’s positive sign, sonography has the advantage over MRI16. Various modalities may facilitate in confirmation of AC diagnosis. The most traditional approach entails the application of ultrasonography (US) and cholecystoscintigraphy (HIDA), or even both to confirm AC’s diagnosis17. CT is used in situations where there is diagnostic dilemma or any complicated cholecystitis detection18. With regards to the case study, the enlarged gallbladder is easily detected through the ultrasound and the CT scan. Cholelithiasis is easily detected through the sonogram as indicated in Figure 2 and Figure 6. Figure 3 indicates gallbladder wall thickening. Figure 4 indicates MRI of acute calculous cholecystitis. Figure 5 indicates acute cholecystitis. The standard signs for CT for the AC’s diagnosis include gallbladder distension, pericholestitic fat’s inflammatory process, pericholecystitic fluid, and thickening of the gallbladder’s wall, which are only described in the CT examinations that are contrast-enhanced19. However, number of signs might be detected in patients that do not have AC. For instance, distension of the gallbladder might take place in prolonged fasting. There may be also pericholecystic strandings once there is neighboring inflammatory process like diverticulitis20. AC diagnosis by CT scan with no contrast enhancement is normally overlooked since gallstones are considered the only finding that is detectable on the CT scan that is unenhanced21. Moreover, gallstones are frequently observed in patients who do not have AC. Eventually, AC diagnosis is grounded on a mixture of clinical signs, imaging techniques and laboratory findings. The diagnosis might be tricky particularly in patients who are critically ill22. Figure 2 arrows indicate gallstone (From Smith et al 2009) Figure 3:CT and ultrasound in 68 year old patient with perforation of the gallbladder. Ultrasound indicates gallbladder wall thickening, dependable with cholecystitis (FromSmith et al 2009). Figure 4 CT Scan showing cholecystitis (From Smith et al 2009) Figure 4. MRI image showing acute calculous cholecystitis (From Smith et al 2009) Figure 5 CT showing acute cholecystitis (From Smith et al 2009) Figure 6. Xray image showing gallstone (From Smith et al 2009) 4. Treatment and Prognosis Patients with AC normally present with pain in the abdomen associated with nausea, vomiting, and fever23. Tenderness and pain are normally localized to the RUQ and this pain might radiate to the right scapula, right clavicular region, or to the back24. There are various factors that influence AC treatment. These include and not limited to the patient’s age, medical history and overall health. The degree of the illness together with the patient’s cooperation in treatment also influences the general treatment. Early diagnosis of AC facilitates prompt treatment and decreases both morbidity and mortality25. The right laparoscopic cholecystectomy’s timing in the management of AC is still controversial26. Previously, early open cholecystectomy was demonstrated as the ideal AC’s management to decrease total stay in the hospital, morbidity, and mortalit27. With laparoscopic surgery’s advent, the advantages of early operation have actually been the issue of argument28. Previous reports indicated that early AC’s laparoscopic surgery was linked to increased rates of complication, prolonged times of operation, and raised conversion rates29. Current evaluation has shown early laparoscopic operation to be an option that is safe in AC, even though conversion to open frequencies might be greater30. On the other hand, there is still no conclusive proof to determine best practice with regards to clinical advantage for delayed or early laparoscopic cholecystectomy among patients who present with AC31. Normally, AC treatment entails hospitalization to minimize gallbladder stimulation. During hospital stay, antibiotics can be administered in order to decrease the inflammation as well as reduce the infection32. Drugs that dissolve stones may be administered as well. With regards to diet, it is imperative to give the patient a diet that is low in fat. Pain management is mandatory so as to enhance patient’s health outcome33. With regards to prognosis, the mortality percentage in patients with AC is 0 to 10 while the mortality percentage in patients who have Acalculous Cholecystitis and postoperative cholecystitis is as soaring as 23 to 4034. In elderly patients, co-morbidity like diabetes might raise the death’s risk. A lot of reports concerning AC’s morbidity and mortality are hard to make comparison since there are considerable variations during the co-morbidities’ presence, diagnostic criteria, timing and kind of operation, hospital systems of support for patients who are critically ill, and variations in surgical expertise available35. 4. Summary and Conclusion In conclusion, Acute Cholecystitis takes place when bile is retained within the gallbladder. However, there are other factors that cause Acute Cholecystitis. With regards to the case study, the main symptom is pain in the RUQ of the abdomen. Other symptoms related to AC include nausea and vomiting. On physical examination, the abdomen is very tender to touch. The laboratory tests related to AC include AST, alkaline phophatase, WBC, and direct bilirubin, all of which are slightly higher than the normal level. The imaging tests also help in diagnosis of AC. This is because they show inflammation or gallstones. Getting immediate medical care is imperative. Even though cholecystitis might disappear by itself, cholecystectomy which is gallbladder removal is normally required in case there is presence of gallstones, as seen in the case study. Nonsurgical treatment for the patient includes and not limited to antibiotics to prevent or fight infections; pain medications; and diet that is low in fat. 5. Bibliography Siddiqui, Tamim, Alisdair MacDonald, Peter S. Chong, and John T. Jenkins. 2008. "Early versus delayed laparoscopic cholecystectomy for acute cholecystitis: a meta-analysis of randomized clinical trials". The American Journal of Surgery. 195 (1): 40-47. Yusoff IF, JS Barkun, and AN Barkun. 2003. "Diagnosis and management of cholecystitis and cholangitis". Gastroenterology Clinics of North America. 32 (4): 1145-68. Cheng, She-Meng, Suk-Ping Ng, and Shin-Lin Shih. 2004. "Hyperdense gallbladder wall sign:An overlooked sign of acute cholecystitis on unenhanced CT examination". Clinical Imaging. 28 (2): 128-131. 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. Kimura Y, T Takada, Y Kawarada, Y Nimura, K Hirata, M Sekimoto, M Yoshida, et al. 2007. "Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines". Journal of Hepato-Biliary-Pancreatic Surgery. 14 (1): 15-26. Portincasa, P., A. Moschetta, M. Petruzzelli, G. Palasciano, A. Di Ciaula, and A. Pezzolla. 2006. "Symptoms and diagnosis of gallbladder stones". Best Practice & Research Clinical Gastroenterology. 20 (6): 1017-1029. Vincent, J. L. 2011. Textbook of critical care. Philadelphia, PA: Elsevier/Saunders. Brown, Anthony F. T., and Michael D. Cadogan. 2006. Emergency medicine: emergency and acute medicine : diagnosis and management. London: Hodder Arnold. Blumgart, L. H., and J. Belghiti. 2007. Surgery of the liver, biliary tract, and pancreas. Philadelphia, PA: Saunders Elsevier. Paran, H, R Zissin, E Rosenberg, I Griton, E Kots, and M 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. Smith EA, JR Dillman, KM Elsayes, CO Menias, and RO Bude. 2009. "Cross-sectional imaging of acute and chronic gallbladder inflammatory disease". AJR. American Journal of Roentgenology. 192 (1): 188-96. Van De Graaff, Kent M., R. Ward Rhees, Sidney L. Palmer, and Kent M. Van De Graaff. 2010. Human anatomy and physiology. New York: McGraw-Hill. Read More
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