WordPress.com



Running head: ACUTE CHOLECYSTITISAcute CholecystitisGCNL 5110 Case Study PaperUniversity of VirginiaSchool of NursingAllyson Vasi CNL Class of 2012Patient SummaryThe case encountered on the Medical-Surgical unit 5 West at the University of Virginia on October 12, 2010 was patient R.F., a 51 year-old male admitted for acute cholecystitis (AC) and postoperative day two from an open cholecystectomy. The patient presented to Pulanski Community Hospital in West Virginia on October 5, 2010 because of sudden onset of right upper quadrant abdominal pain and nausea without vomiting. R. F. rated his pain level using a standardized pain scale as a 10/10. At that time, the patient received Dilaudid which helped to reduce his pain to a 6/10. The pain radiated from his right upper quadrant to his epigastrium. The patient subsequently transferred to the University of Virginia Medical Center on October 9, 2010 because CT imaging revealed air in the biliary tree and a distended gallbladder. On October 10, 2010, the patient had an open cholecystectomy which revealed cholecystitis. The patient’s previous medical and surgical history consists of hypertension, hypercholesterolemia, chronic obstructive pulmonary disease (COPD), depression, anxiety, a cervical spinal fusion, a lumbar spinal fusion, a gunshot wound (GSW) to the lower abdomen, a percutaneous coronary artery stent, and a right knee fracture. The patient’s health status at the time of assessment showed stable vital signs with acute abdominal pain related to his surgery which he rated using the U. Va. Pain Scale as a 10/10. R. F. received as needed Percocet for the pain; however, he continued to be dissatisfied with the level of his pain and comfort. R.F. was alert and oriented to person, place, and time, was able to communicate his needs, and his movement was purposeful to his pain. His gait was unsteady and his range of motion was limited. He had stand-by assistance as well as wheelchair accessibility to help in his movements. His hearing, speech, and vision were all normal, eyes were clear and moist and free of edema and discharge, oral mucosa was pink and moist and teeth were intact. The patient’s breath sounds revealed decreased bases with rhonci, O2 at 2L/min was required intermittently via nasal cannula with use of an incentive spiromenter, and there was an absence of breathing difficulty, cough, pain with inspiration, and retractions. There were no visible pulsations over the pericardium; the point of maximal impulse was palpable at the fifth intercostals in the midclavicular line, 1 cm in diameter. There were no lifts, heaves, or thrills felt on palpitation. S1 and S2 were present without murmur and skin was warm and dry. Capillary refill was less than three seconds and there was absence of cyanosis and chest pain. There was 2+ edema in the lower extremities bilaterally and the patient was receiving pharmacological deep-vein thrombosis prophylaxis. The patient’s abdomen was firm and distended with no masses upon superficial palpation, and his bowel sounds were hypoactive. R.F. denied nausea, vomiting, constipation, and diarrhea, and there was an absence of rectal and oral bleeding. R.F. was voiding regularly with no urinary devices and his urine was a clear-pale yellow with no odor. He had a bowel movement within the last 24 hours and was on a clear-liquid diet preoperative which had changed to a regular diet on this day. The patient’s genitalia were intact without discharge, swelling, or pain, and there was no bladder distention.The patient’s care during the experience primarily focused on his surgical wounds and pain control. Further, his hospital course plan consisted of discharge teaching and pain management teaching. R.F. would be able to return to his home in the next couple of days if he showed adequate learning and understanding of his medications and surgical wound care, and if his pain management regimen was sufficient and able to control his pain levels. R.F. would return home with his wife who would be his primary caregiver and who would help with his adherence to his medication regimen and wound care.Overall, R.F. was anxious and agitated at the beginning of the clinical experience due to his levels of pain and lack of understanding related to his healing. Once he received education on the healing of his surgical wounds and how to get his pain under control, he was pleasant and cooperative. R.F. and his wife understood and responded well to the procedures necessary to prepare him for discharge. PathophysiologyAcute Cholecystitis (AC) is inflammation of the gallbladder caused by gallstones that have obstructed the cystic duct. There are two types of AC that can occur, calculous and acalculous. The most common type is calculous which is observed in this patient. Calculous AC occurs in response to chemical irritation and inflammation from gallstones that obstruct the cystic duct, as seen in this patient, or obstruction of the gallbladder neck or common bile duct. When the gallbladder is inflamed, trapped bile is reabsorbed and acts as a chemical irritant to the gallbladder wall. Reabsorbed bile along with impaired circulation, edema, and distention of the gallbladder causes ischemia and infection. All of these occurrences combined result in tissue sloughing and necrosis and gangrene as observed in this patient. The gallbladder wall may eventually rupture, with possible formation of an abscess (Huffman & Schwenker, 2010). The pathophysiology of gallstone formation is not clearly understood but recent literature has reported abnormal metabolism of cholesterol and bile salts as potential contributors. Gallstones are crystalline structures formed by the concentration of normal or abnormal bile constituents. There are three types of gallstones: cholesterol, pigmented, and mixed. Cholesterol stones account for 80% of the stones found in Americans; however, only about 10% of these are pure cholesterol. Most stones are of mixed composition and also contain calcium salts, bile acids, fatty acids, phospholipids, and bile pigments. Pigmented gallstones account for 20% of stones and are composed primarily of calcium bilirubinate. Multiple stones are present in about two-thirds of all patients. In patients with single stones, 50% have gallstones that are less than 2 cm in diameter. In patients with multiple stones, 80% of those patients have gallstones that are less than 2 cm in size (Barbara, Sama, Labate, Taroni, Rusticali, Festi, et al., 1987). The formation of gallstones can occur because of bile stasis and sludge. Volume depletion leads to concentration of bile which can thicken in the absence of a stimulus for gallbladder emptying. This results in a buildup of bile that can cause inflammation. Several early clinical studies suggested that ileus can result in bile stasis, but experimental results are conflicting (Barie & Eachempati, 2010). Another way bile stasis can occur is by mechanical ventilation with positive end-expiratory pressure, which also decreases portal perfusion by increasing hepatic venous pressure. Sludge is a cholesterol-rich material that is common when there is hypocontractility of the gallbladder and may represent an early stage of gallstone formation. Proposed mechanisms for development of bile buildup sludge include bile stasis, hypocontractility of the gallbladder, secondary bacterial and fungal infections, and ischemia. (Angelico, De Santis, & Capocaccia, 1990). Gallbladder ischemia also plays a central role in the pathophysiology of acute cholecystitis, with a relationship between ischemia and stasis possibly leading to hypoperfusion. Dehydration, hypotension, or the administration of vasoactive drugs can decrease perfusion, whereas intraluminal pressure is increased by bile stasis, thereby decreasing gallbladder perfusion pressure. Clinical observations of hypoperfusion leading to AC support the hypothesis of decreased microcirculation with cellular hypoxia as a fundamental cause of AC, as does the pathologic observation of high rates of gallbladder necrosis and perforation. Further, AC is associated with multiple arterial occlusions and minimal-to-absent venous filling, supporting the hypothesis that vascular occlusion and microcirculatory disruption plays a role in the pathophysiology of AC (Barie & Eachempati, 2010). Vasoactive mediators are observed in the pathophysiology of acute cholecystitis as well. The host response to gram-negative bacteremia or splanchnic ischemia-reperfusion is the primary relation with bacterial infection occurring as a secondary phenomenon, as seen in this patient. In AC, bile (which is normally sterile) will contain bacteria in 50% to 75% of patients. While not all cases of AC are associated with bacterial colonization of the bile, almost all deaths are due to septic complications of the disease. Intravenous injection of Escherichia coli lipopolysaccharide, which mimics clinical sepsis, produced AC in several mammalian species during clinical experiments. Further, platelet-activating factor has been recognized in the pathophysiology of splanchnic hypoperfusion in sepsis and other low-flow states. The inflammation seems to be mediated by proinflammatory eicosanoids, because it is inhibited by nonspecific cyclooxygenase inhibitors (Barie & Eachempati, 2010). Risk factors for acute cholecystitis include previous or current gallstones, as seen in this patient, traumatic injury to the abdomen, also seen in this patient, diabetes, long labor, immunosuppression, and obesity. End-stage renal disease is associated with cholecystitis perhaps because both diabetes and atherosclerosis are common in patients with end-stage renal disease who often experience low flow on hemodialysis (Barie & Eachempati, 2010). Patients with cancer are also at risk for cholecystitis, and it has been reported in patients with acute myelogenous leukemia. Acute cholecystitis may also develop as a secondary infection of the gallbladder during systematic sepsis with reported cases occurring with malaria, brucellosis, Q fever, and dengue fever (Bahl, Berry, Dull, Zimny, Noureldin, Roe, et al., 2010). Viral pathogens associated with cholecystitis include hepatitis A and B (Unal, Korkmaz, Kirbas, et al., 2009; Souza, Braga, Rocha, et al., 2009), and the Epstein-Barr virus (Iaria, Leonardi, Fabiano, et al., 2009). Signs and symptoms include steady pain the right upper quadrant, radiating pain from the abdomen to the right shoulder or back, tenderness of the abdomen upon palpation, sweating, nausea, vomiting, anorexia, fever, chills, and abdominal bloating. A patient presenting with acute cholecystitis may have a mild fever with mild tachycardia; however if perforation and/or generalized sepsis has occurred the patient may present with a high fever, chills, rigors, and confusion in association with hypotension and severe tachycardia. The patient presented with a number of these signs and symptoms including right upper quadrant pain, radiating pain, tenderness upon palpation, and nausea. Many of these signs and symptoms tend to occur after a meal especially if the meal was high in fat (Baltimore & Davidson, 2007). Medical ManagementNo single laboratory test can establish or rule out a diagnosis of acute cholecystitis without further testing. An abdominal ultrasound or CT scan, which was performed for this patient, is the preferred initial investigation and can accurately detect cholecystitis in up to 95% of patients presenting with biliary pain and may also detect other abnormalities that assist in the diagnosis. Also, a hepatobiliary iminodiacetic acid (HIDA) scan can show a picture of the liver, gallbladder, biliary tract, and small intestine and can track the flow of bile from the liver to the small intestine revealing if there is blockage at any point. (Baltimore & Davidson, 2007). Diagnostic tests include a total bilirubin measurement, which if elevated may indicate biliary tract involvement and may indicate more severe bile duct pathology such as cholangiocarcinoma (Baltimore & Davidson, 2007). A white blood cell count which is elevated in 85% of patients with cholecystitis, along with an elevation in serum alkaline phosphatase, may be useful in aiding the diagnosis of cholecystitis, but only when used in conjunction with patient history, physical exam, and other diagnostic tests (Trowbridge, Rutkowski, & Shojania, 2003). Other diagnostic tests include aspartate aminotransferase and alanine aminotransferase which are elevated in 40% to 75% of cases of acute cholecystitis, even without common bile duct obstruction or cholangitis (Patwardhan, Smith, & Famelant, 1987). Finally, in the presence of clinical symptoms, abnormal cholescintigraphy results aid in the diagnosis of acute cholecystitis (Bellows, Berger, & Crass, 2005). The patient presented with elevation in many of these diagnostic tests including an elevation in white blood cell count, elevation in serum alkaline phosphatase, along with aspartate aminotransferase and alanine aminotransferase elevation. The diagnosis of acute cholecystitis is based on the presence of at least two of three factors including (1) acute right upper quadrant tenderness, (2) fever higher than 37.5 ° C, or leukocytosis greater than 10,000/mm, and (3) ultrasound and/or CT evidence such as thickened and edematous gallbladder wall, the presence of maximal tenderness elicited over a sonographically localized gallbladder, and pericholecystic fluid collection (Baltimore & Davidson, 2007). The patient presented with at least two of these characteristics including acute right upper quadrant pain and tenderness upon palpation, and a CT image revealing a distended gallbladder and air in the biliary tree. Most patients with acute cholecystitis do not respond to medical management and an early cholecystectomy can improve patient outcomes. Surgery may be immediately indicated if complications such as necrosis have occurred. A percutaneous cholecystostomy is the treatment of choice, but response to drainage may not be prompt or favorable and abdominal exploration is adamant. A cholecystectomy is most commonly performed laparoscopically, distributing the tissue notably less than open surgery, and resulting in less postoperative pain and a quicker recovery (Balitmore & Davidson, 2007; Gilbert, Moellering, Eliopoulos, et al., 2005). Cholecystectomy by either technique does not decompress the common bile duct if cystic duct obstruction is present, therefore the common duct must be decompressed by some other method, such as an open common bile duct exploration. Patency of the cystic duct can be determined immediately by tube cholangiography, which should always be performed after the patient has recovered to determine the presence of gallstones that may have not been detected (Baltimore & Davidson, 2007).Patients suspected to have acute cholecystitis should be hospitalized and started on broad spectrum antibiotics immediately. Antibiotic therapy does not substitute for drainage of AC, but it is an important adjunct. The most common bacteria isolated from bile in AC are E. Coli, Klebsiella spp, and Enterococcus faecalis. Antibiotic therapy should be directed against these organisms. Critical illness and prior antibiotic therapy alter host flora, however, and resistant or opportunistic pathogens may be encountered. Recommended regimens include piperacillin/tazobactam, ticarcillin/clavulanate, ertapenem, meropenem, and ampicillin/sulbactam. Imipenem/cilastatin is recommended for life-threatening cases and pain should be treated along corrections of any electrolyte imbalances (Barie, Hydo, Pieracci, et al., 2009). Most people who have gallstones will not develop complications requiring treatment. However, those who do develop symptoms related to gallstones should be treated immediately because these patients are at risk for serious complications. In general, the overall prognosis for cholecystitis is fair. Acute cholecystitis has the highest morbidity (55%) and mortality (30% to 40%) of all nonmalignant conditions affecting the gallbladder. Early diagnosis with rapid intervention is critical to improving outcomes (Shapiro, Luchtefeld, Kurzweil, et al., 1994; Frazee, Nagorney, & Mucha, 1989; Fox, Wilk, Weissmann, et al., 1984). Elderly patients with cholecystitis have an increased morbidity and mortality, a higher conversion rate to open cholecystectomy, and present more frequently with complications including biliary pancreatitis, choledocholithiasis, and acute cholecystitis (Pessaux, Tuech, Derouet, et al., 2000; Borzellino, de Manzoni, Ricci, et al., 1999). All patients with cholecystitis should be admitted to the ICU and surgical consultation should be requested for any patient with cholecystitis (Bellows, Berger, & Crass, 2005).Further medical management for this patient consisted of administration of a broad-spectrum antibiotic prior to surgery, followed by an open cholecystectomy revealing acute gangrenous cholecystitis. Nursing ManagementThe nursing management for suspected acute cholecystitis should begin with measures to prepare the patient for possible surgery. It is important to obtain an order for an antibiotic immediately while in preparation for surgery. The patient is to be kept N.PO. with administration of IV fluids as ordered. Measurement of intake and outputs are necessary with administration of electrolyte replacement and antiemetics if the patient is vomiting. As ordered, antibiotics and analgesics should be administered. A preoperative patient assessment is important to establish that the patient is fit for surgery. It is the role of the nurse to ensure that the patient is well informed about the procedure, as well as to help the patient deal with any anxiety. The nurse should be prepared for their role in managing preoperative anxiety so that they can act as an advocate for patients. Good documentation also plays a pivotal role in effective preoperative assessments, which along with effective communication will ensure that the ward and patient teams are able to plan and subsequently deliver individualized patient care (Graham, 2008). The observed patient received much of the above mentioned care, with well documented preoperative assessments including intake and outputs, ordered antibiotics, IV fluids and N.PO. diet. It is important for the nurse to recognize that many patients will have significant co-morbidities associated with gallstones such as obesity and hypercholesterolemia, as seen in this patient. These co-morbidities can have significant influence on the risks associated with anesthesia and should be discussed with the patient prior to surgery. The aim of preoperative assessment for patients awaiting a cholecystectomy is to ensure that no further complications associated with gallbladder or gallstone disease develop, and that the overall surgery remains as routine as possible. The preferred surgical procedure for acute cholecystitis is a laparoscopic cholecystectomy; however an open cholecystectomy may be performed if laparoscopY is contraindicated due to chronic lung disease, as seen in this patient, or heart failure. The procedures are usually performed under general anesthesia. The most commonly used general anesthetic is the induction of propofol, paralysis with a muscle relaxant, and an endotracheal tube or laryngeal mask, followed by intermittent positive pressure ventilation. Maintenance of anesthesia is provided by inhalational agents such as desflurance, sevoflurane or by proprofol infusion. The use of nitrous oxide is contraindicated for laprascopic surgery because of evidence finding an increase in the size of the pneumoperitoneum and subsequently an increase in postoperative nausea and vomiting (Graham, 2008). Although minimally invasive, a laparoscopic cholecystectomy has specific complications associated with it. Nursing care while preparing a patient for the operation focuses on appropriate monitoring, securing access to a large bore IV and facilities for central venous placement, and resuscitation equipment. The procedure takes about 60-90 minutes depending on the difficulty of the procedure and whether the patient has a history of previous acute cholecystitis or pancreatitis. The patient is placed in reverse Trendelenburg position, and an important nursing management consideration is awareness of possible venous stasis that may occur. Deep vein thrombosis prophylaxis is therefore indicated with use of compression stocking and boots to improve venous return. Carbon dioxide is administered to distend the abdomen allowing adequate visualization of the cavity to avoid injury to internal organs. Nursing management requires maintaining the carbon dioxide at the lowest possible pressure (less than 12mmHg), evading inferior vena cava compression which could lead to circulatory collapse and prevent diaphragmatic splinting that affects mechanical ventilation (Blay & Donoghue, 2006). A fibreoptic telescope is inserted through a trocar into the peritoneal cavity, with a camera attached allowing the surgeon to view the instruments and the surgical field. After dissection of the gallbladder, the surgeon clips the cystic artery and duct, then withdrawS the gallbladder from the liver bed through an umbilical incision. Local infiltration of the wounds and intraperitoneal local anesthesia is then administered following the procedure. Laparoscopic cholecystectomy is shown to be associated with intra-abdominal, incisional, and shoulder pain after surgery. It appears that a significant reduction is observed, however, when intraperitoneal local anesthetic is also infiltrated into the incisions. Because postoperative shoulder pain is associated with the size of the residual gas bubble under the diaphragm, releasing as much carbon dioxide as possible from the abdomen is an important nursing consideration as well. Possible complications with surgery include bile leakage, fluid collection in the abdomen, bleeding, and bile duct injury (Graham, 2008). Laparoscopic cholecystectomy is contraindicated for patients with chronic lung disease observed in this patient, or heart failure, because these patients cannot tolerate the carbon dioxide used in the laparoscopic procedure. Therefore a traditional open cholecystectomy is performed. The nurse provides preoperative care and teaching, and the surgeon removes the gallbladder through a large incision, while also exploring the biliary tract ducts for gallstones. During surgery, the placement of a Jackson-Pratt (JP) drain is inserted to prevent fluid accumulation (Blay & Donoghue, 2006). Postoperative nursing care for both procedures requires close monitoring after the operation. The patient is first placed in a recovery area after surgery where they are to be closely monitored for several hours until their condition is determined to be stable. Nurse monitoring includes vital signs, pain ratings, levels of postoperative nausea and vomiting, wound sites and wound drain care. Additional risk factors the nurse should be aware of during postoperative care include female gender, previous postoperative nausea and vomiting or motion sickness, and the use of perioperative opioids. Postoperative nausea and vomiting is common in the immediate recovery period, resolving after one to two days. Opioids are a common cause of postoperative nausea and vomiting, and should be kept to the required minimum. Antiemetic prophylaxis is encouraged and can help in stabilization of the patient. Adequate hydration is also a concern for the nurse, with the patient receiving at least one liter of IV fluid during the procedure as an important consideration to reduce postoperative nausea and vomiting. If the patient does experience postoperative nausea and vomiting, it should be treated promptly using a different class of antiemetic than that used for prophylaxis. Pain after any surgery is expected, despite prophylactic multimodal analgesia administration. Patients are most likely to require some form of opioid analgesia during their recovery and possibly a prescription for regular dosing oral analgesia before discharge. Nursing management requires the nurse to be aware that pain is usually moderate to severe during the first couple of postoperative days, hopefully reducing after that, but can still be severely intense preventing early discharge. Referred pain to the tip of the shoulder and/or back is also likely to occur as a result of insufflations of carbon dioxide into the abdominal cavity or irritation of the diaphragm (Graham, 2008). Non-steroidal anti-inflammatory drugs (NSAIDs) and other non-opioids should be considered for reduction of postoperative pain intensity, but are usually inadequate alone. Intraperitoneal instillation of local anesthetics can be used in the immediate postoperative period for pain reduction, as well as infiltrating the insertion sites with local anesthetic. Unfortunately, none of these drugs are effective in treating referred pain. Based on this, the most effective analgesic regimen for the nurse to consider consists of preoperative prophylactic administration of a non-opioid, preoperative infiltration of the skin incision sites with local anesthesia, the instillation of a local anesthetic into the upper abdomen before abdominal closure and administration of an opioid for postoperative pain. It is vital that nursing care provides patients with information about their analgesic regimen and wound care before discharge (Blay & Donoghue, 2006). By providing patients with practical discharge information on these topics, along with information about returning to daily activities and dietary advice, it will improve patient confidence and reduce any possible anxieties about managing their home care. Patients should also be warned of possible complications and when to contact their health care provider if relating signs and symptoms occur. It is an important aspect of nursing care to ensure the patient has adequate support following discharge, whether this is the identification of a primary care giver, a postoperative telephone call from the nurse or surgical team, along with adequate follow up from physical and occupational therapists. These postoperative considerations following surgery can help to significantly reduce anxiety and pain levels (Graham, 2008). It is imperative that the nurse recognizes unique needs of the patients they are caring for and how factors like age and additional risk factors can influence the recovery period. Elderly patients have an increased morbidity and mortality, a higher conversion rate to open cholecystectomy, and present more frequently with complications. The observed patient is relative young, but has a significant co-morbidity associated with gallstones and, hypercholesterolemia. This will have a significant influence on the risks associated with anesthesia and may increase his hospital stay. SummaryAcute cholecystitis should be expected in any critically ill patient presenting with sepsis, and for whom the source of infection is not immediately identified. Suspicion should be high if the patient is injured, has undergone recent major surgery, has had a period of hypotension, or hypoperfusion, or becomes jaundice. Ultrasound and CT scans are the preferred diagnostic tools and are inexpensive, noninvasive, and can be brought to the bedside. Broad-spectrum antibiotics should be considered and immediately administered once ordered. Once diagnosed, the preferred treatment is percutaneous cholecystectomy, but if the response to drainage is not prompt and favorable, an alternative diagnosis should be considered, and an abdominal exploration performed. If percutaneous drainage is successful and the patient is found to have no gallstones, then no further treatment may be necessary. If unsuccessful, with abdominal exploration revealing cholecystitis, a laparoscopic cholecystectomy is preferred for removal of the gallbladder, but if contraindicated, an open cholecystectomy may be performed. Postoperative care revolves around stabilizing the patient and adopting an adequate pain management regimen. Discharge teaching should be provided including information on pain management, wound care, and information about returning to daily activities and dietary advice. Follow-up with the patient after discharge should be made to reduce any possible anxieties. ReferencesAngelico, M., De Santis, A., & Capocaccia, L. (1990). Biliary sludge: A critical update. Journal of Clinical Gastroenterology, 12, 656-662.Bahl, A., Berry, B., Dull, B., Zimny, M., Noureldin, T., Roe, J., Swor, R. (2010). Laboratory evaluation in diagnosis of cholecystitis. Annals of Emergency Medicine, 56, 36. Baltimore, J. J., & Davidson, J. (2007). Caring for a patient with acute cholecystitis. Hospital Nursing, 37, 64-66. Barbara, L., Sama, C., Labate, A., Taroni, F., Rusticali, A., Festi, D., Sapio, C., et al. (1987): A population study on the prevalence of gallstone disease: The sermione study. Hepatology,7, 913.Barie, P. S., & Eachempati, S. R. (2010). Acute cholecystitis. Gastroenterology Clinics, 39, 343-357Barie, P. S., Hydo, L. J., Pieracci, F. M., et al. (2009). Multiple organ dysfunction syndrome in critical surgical illness. Surgical Infections, 10, 369-377.Bellows, C.F., Berger, D.H., & Crass, R.A. (2005). Management of gallstones. American Family Physician, 72, 637-642.Bhansali, S.K. (1985). Preoperative complications of gallstones and their relevance to treatment and prognosis: Experience with 451 cases. American Journal of Gastroenterology, 80, 648-654. Blay, N., & Donoghue, J. (2006). Source and content of health information for patients undergoing laparoscopic cholecystectomy. International Journal of Nursing Practice, 12, 64-70. Borzellino, G., de Manzoni. G., Ricci, F., et al. (1999). Emergency cholecystostomy and subsequent cholecystectomy for acute gallstone cholecystitis in the elderly. British Journal of Surgery, 86, 1521-1525.Fox, M.S., Wilk, P.J., Weissmann, H.S., et al. (1984). Acute acalculous cholecystitis. Surgery, Gynecology, & Obstetrics Journal, 159, 13-16.Frazee, R.C., Nagorney, D.M., & Mucha, P. Jr. (1989). Acute acalculous cholecystitis. Mayo Clinic Procedings, 64, 163-167.Gilbert, D.N., Moellering, R.C. Jr., Eliopoulos, G.M., et al (Eds): The Sanford Guide to Antimicrobial Therapy 2005, 35th ed. Antimicrobial Therapy, Inc, Hyde Park, VT, USA, 2005.Graham, L. (2008). Care of patients undergoing laparoscopic cholecystectomy. Nursing Standard, 23, 41-48. Huffman, J. L., & Schwenker, S. (2010). Acute acalculous cholecystitis: A review. Clinical Gastroenterology and Hepatology, 8, 15-22. Iaria, C., Leonardi, M. S., Fabiano, C., et al. (2009). Acalculous cholecystitis during the course of acute Epstein-Barr virus infection and Gilbert’s syndrome. International Journal of Infectious Diseases, 13, 519-520. Patwardhan, R.V., Smith, O.J., & Farmelant, M.H. (1987). Serum transaminase levels and cholescintigraphic abnormalities in acute biliary tract obstruction. Archieves of Internal Medicine, 147, 1249-1253.Pessaux, P., Tuech, J.J., Derouet, N., et al. (2000). Laparoscopic cholecystectomy in the elderly: A prospective study. Surgical Endoscopy, 14, 1067-1069.Shapiro, M.J., Luchtefeld, W.B., Kurzweil, S., et al. (1994). Acute acalculous cholecystitis in the critically ill. American Journal of Surgery, 60, 335.Souza, L. J., Braga, L. G., Rocha, S., et al. (2009). Acute acalculous cholecystitis in a teenager with hepatitis A viral infection : A case report. Brazil Journal of Infectious Diseases, 13, 74-76. Trowbridge, R. L., Rutkowski, N.K., & Shojania, K.G. (2003). Does this patient have acute cholecystitis? Journal of American Medical Association, 289, 80-86.Unal, H., Korkmaz, N., Kirbas, I., et al. (2009). Acute acalculous cholecystitis associated with acute hepatitis B infection. International Journal of Infectious Diseases, 13, 310-312. ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download