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Your search term(s) "Thrombocytosis or thrombosis" returned 95 results.

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Surgical Techniques in Right Laparoscopic Donor Nephrectomy. Journal of the American College of Surgeons. 195(1): 131-137. July 2002.

The benefits of laparoscopic donor nephrectomy (LDN, removal of a donated kidney using laparoscopic, rather than open surgery, techniques) have been well described, but limitations in the technical performance of LDN of the right kidney have isolated its performance to only a few advanced laparoscopic centers. This article reviews the technical challenges of right LDN and offers several approaches for improving the right LDN technique. Topics include port placement and liver retraction, inferior vena caval dissection, arterial mobilization, division of the renal vessels, and anticipated results of the procedure. The authors conclude by noting that a considerable proportion of living donors should undergo right rather than left donor nephrectomy for anatomical reasons, including multiple renal arteries, smaller right kidney, or undiagnosed lesions within the right donor kidney. The ability to perform right LDN allows the inclusion of those donors with only right kidneys suitable for donation. When the operation is performed with attention to potential complications, right LDN can provide kidneys without increased risk for thrombosis or other technical complications. 1 table. 6 figures. 13 references.

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Vascular Access: Anatomy, Examination, Management. Seminars in Nephrology. 22(3): 183-194. May 2002.

A systematic approach to managing vascular access (VA) problems in hemodialysis patients is the key to reducing current high rates of access thrombosis (clotting) and failure. This article describes this systematic approach that consists of anatomy, examination, and management. The approach begins with a thorough knowledge of vascular access anatomy that, when combined with the physical examination, can help optimize access planning and maintenance. Because of the high complication rate of synthetic grafts, there has been increased emphasis on creating autogenous (from the patient herself or himself) arteriovenous (AV) fistulae, which, once established, are more trouble-free. The benefit of increased fistula creation will not be realized, however, until the high rate of early fistula failure is reduced. It is widely recommended that graft surveillance programs be implemented and that stenosis (narrowing) be corrected when accompanied by graft dysfunction. Graft blood flow is the preferred surveillance method, but has a poor accuracy in predicting thrombosis. The authors conclude that the most important factor in access survival may be a team approach with an organized commitment to access planning, followed by recognition and treatment of access problems. 2 figures. 7 tables. 64 references.

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Vascular Access: Principles and Practice. 4th ed. St. Louis, MO: Mosby, Inc. 2002. 289 p.

This text reviews the principles and practice of vascular access, including that used for hemodialysis and for critical care, chemotherapy, and nutrition. The text features 25 chapters that cover: the development of vascular access (VA) surgery, planning and patient assessment, anesthesia, surgical anatomy for VA procedures, physiology for the arteriovenous fistula, biologic properties of VA devices, biologic response to prosthetic dialysis grafts, epidemiology of chronic renal (kidney) failure (CRF) and guidelines for the initiation of hemodialysis, autologous arteriovenous fistulas, basilic vein transposition, vascular interposition (bridge fistulas) for hemodialysis, central venous cannulation for hemodialysis access, vascular access in the neonatal and pediatric patient, revision and outcome of VA procedures for hemodialysis, radiologic intervention and instrumentation for the salvage of hemodialysis access grafts, axillosubclavian vein thrombosis (clotting), thrombosis, venous hypertension, arterial steal, and neuropathy (nerve disease or damage), complications of VA procedures, care and use of VA devices, cardiovascular consequences of rapid hemodialysis, peritoneal dialysis, socioeconomic implications of VA surgery, placement of indwelling VA systems, VA for trauma and emergency surgery, and complications of percutaneous VA procedures and their management. Each chapter includes black and white illustrations and a list of references; a subject index concludes the volume.

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Chronic Pancreatitis. In: Beckingham, I.J., ed. ABC of Liver, Pancreas and Gallbladder. London, UK: BMJ Publishing Group. 2001. p.37-40.

Chronic pancreatitis is usually caused by alcohol misuse and it mainly affects men aged 40 to 50 years. There is no uniform threshold for alcohol toxicity, but the quantity and duration of alcohol consumption correlates with the development of chronic pancreatitis. This chapter on chronic pancreatitis is from an atlas of the liver, pancreas and gallbladder. Topics include natural course, symptoms and signs, diagnosis, treatment options (for pain, steatorrhea, and diabetes), endoscopic procedures, surgery, and complications of chronic pancreatitis, including pseudocysts, biliary stricture, gastroduodenal obstruction, and splenic vein thrombosis. The authors note that early diagnosis of chronic pancreatitis is often difficult and relies on appropriate clinical history and imaging. Stopping alcohol intake is essential to reduce attacks of pain, preserve pancreatic function, and aid management of complications. Patients often require opiate analgesics (painkillers), and pain is best managed in a multidisciplinary setting. Surgery should be reserved for patients with intractable pain or with complications. The chapter concludes with summary points of the concepts discussed. 7 figures. 2 tables. 3 references.

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Clinical Outcomes and Insulin Secretion After Islet Transplantation with the Edmonton Protocol. Diabetes. 50(4): 710-719. April 2001.

This article provides further data on 12 patients with type 1 diabetes who have had successful islet transplantations. Details of metabolic control, acute complications associated with islet transplantation, and long term complications related to immunosuppression therapy and diabetes were noted. Insulin secretion, both acute and over 30 minutes, was determined after intravenous glucose tolerance tests (IVGTTs). The median follow up was 10.2 months, and the longest was 20 months. Glucose control was stable, with pretransplant fasting and meal tolerance stimulated glucose levels of 12.5 plus or minus 1.9 and 20.0 plus or minus 2.7 mmol per liter, respectively, but decreased significantly, with posttransplant levels of 6.3 plus or minus 0.3 and 7.5 plus or minus 0.6 mmol per liter, respectively. All patients had sustained insulin production, as evidenced by the most current baseline C-peptide levels of 0.66 plus or minus 0.06 nmol per liter, increasing to 1.29 plus or minus 0.25 nmol per liter after the meal tolerance test. The mean glycosylated hemoglobin (HbA1c) level decreased from 8.3 plus or minus 0.5 percent to the current level of 5.8 plus or minus 0.1 percent. Four patients had normal glucose tolerance, five had impaired glucose tolerance, and three had postislet transplant diabetes. Three patients had a temporary increase in their liver function tests. One patient had thrombosis of a peripheral branch of the right portal vein, and two of the early patients had bleeding from the hepatic needle puncture site; however, these problems were resolved. Two patients had transient vitreous hemorrhages. The two patients with elevated creatinine levels posttransplant had a significant increase in serum creatinine in the long term, although the mean serum creatinine of the group was unchanged. Cholesterol increased in five patients, and lipid lowering therapy was required for three patients. No patient has developed cytomegalovirus infection or disease, posttransplant lymphoproliferative disorder, malignancies, or serious infection to date. None of the patients have been sensitized to donor antigen. In 11 of the 12 patients, insulin independence was achieved after 9,000 islet equivalents (IEs) per kilogram were transplanted. The acute insulin response and the insulin area under the curve (AUC) after IVGTT were consistently maintained over time. The insulin AUC from the IVGTT correlated to the number of islets transplanted, but more closely correlated when the cold ischemia time was taken into consideration. Islet transplantation has successfully corrected labile type 1 diabetes and problems with hypoglycemia, and results show persistent insulin secretion. After a minimum of 9,000 IEs per kilogram are provided, insulin independence is usually attained. An elevation of creatinine appears to be a contraindication to this immunosuppressive regimen. When considering islet transplantation for people with labile type 1 diabetes that is difficult to control, the risk to benefit ratio should be in favor of islet transplantation. 6 figures. 35 references. (AA-M).

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Diabetes and Atherosclerosis. In: Johnstone, M.T. and Veves, A. Diabetes and Cardiovascular Disease. Totowa, NJ: The Humana Press, Inc. 2001. p. 169-194.

With over ten million diagnosed patients and another five million undiagnosed, diabetes mellitus and its complications is a major public health problem that will assume epidemic proportions as the population grows older. This chapter on diabetes and atherosclerosis (hardening and narrowing of the arteries) is from a textbook that offers physicians practical knowledge about cardiovascular disease and diabetes. This chapter is in Part I, which focuses on pathophysiology, including the mechanisms and risk factors for diabetic cardiovascular disease. The author notes that macrovascular (large vessel) disease is the leading cause of mortality (death) and morbidity (illness) in diabetes. The author discusses endothelial (the cells that line the body cavity and the cardiovascular system) dysfunction, the mechanisms of foam cell formation, the role of humoral immunity and macrophage activation, abnormalities in platelet function, coagulation, and fibrinolysis, particularly as they contribute to thrombus (clot) formation. The author provides updated information concerning factors associated with diabetes that may accelerate the development of atherosclerosis and thrombosis and contribute to acute clinical events. 1 figure. 227 references.

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Diabetes and Cardiovascular Disease. Totowa, NJ: The Humana Press, Inc. 2001. 458 p.

With over ten million diagnosed patients and another five million undiagnosed, diabetes mellitus and its complications is a major public health problem that will assume epidemic proportions as the population grows older. This textbook offers practicing physicians the day to day practical knowledge about cardiovascular disease and diabetes. The 24 chapters in the book focus on either clinical or basic aspects of diabetes and cardiovascular disease. Part I, pathophysiology, reviews the mechanisms and risk factors for diabetic cardiovascular disease. Specific topics include the effects of insulin on the vascular system, vascular abnormalities in the prediabetic state, diabetes and advanced glycation end products, diabetes and hypertension (high blood pressure), the renin-angiotensin system, diabetes and dyslipidemia (disordered levels of fats in the blood), diabetes and thrombosis (blood clotting), diabetes and atherosclerosis (hardening and narrowing of the arteries), and nitric oxide and its role in diabetes mellitus. Part II focuses on the heart in diabetes mellitus, including coronary artery disease and congestive heart failure, including the preoperative assessment and perioperative management of the surgical patient with diabetes mellitus. Part III, the peripheral vascular system, addresses epidemiology (incidence and prevalence), mechanisms, methods of assessment, and treatment of this macrovascular disease. Specific topics include diabetes and arterial stiffness, methods for assessing large vessel pathophysiology, and peripheral vascular disease in patients with diabetes mellitus. And Part IV reviews the different microvascular effects in individuals with diabetes mellitus, including retinopathy (eye disease), nephropathy (kidney disease), neuropathy (nerve disease), and microcirculation of the diabetic foot. Each chapter includes extensive references and a subject index concludes the text.

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Diabetes and Thrombosis. In: Johnstone, M.T. and Veves, A. Diabetes and Cardiovascular Disease. Totowa, NJ: The Humana Press, Inc. 2001. p. 149-168.

With over ten million diagnosed patients and another five million undiagnosed, diabetes mellitus and its complications is a major public health problem that will assume epidemic proportions as the population grows older. This chapter on diabetes and thrombosis (clotting) is from a textbook that offers physicians practical knowledge about cardiovascular disease and diabetes. This chapter is in Part I, which focuses on pathophysiology, including the mechanisms and risk factors for diabetic cardiovascular disease. The authors note that complications of macrovascular disease, referred to by some as atherothrombosis, are responsible for 50 percent of the deaths in patients with type 2 diabetes mellitus, 27 percent of the deaths I patients with type 1 diabetes for 35 years or less, and 67 percent of the deaths in patients with type 1 diabetes for 40 years or more. The authors focus on type 2 diabetes in their discussion of thrombosis and atherosclerosis, platelet function in subjects with diabetes mellitus, the coagulation system and diabetes mellitus, mechanisms responsible for a prothrombotic state associated with diabetes, diabetes and fibrinolysis, mechanisms responsible for the overexpression of PAI (plasminogen activator inhibitor) in diabetes, fibrinolysis and arterial mural proteolysis, and therapeutic implications. The authors conclude that subjects with diabetes mellitus have a high prevalence and rapid progression of coronary artery, peripheral vascular, and cerebral vascular disease secondary in part to increased platelet reactivity, increased thrombotic activity and decreased activity of antithrombotic factors, and decreased fibrinolytic system capacity. Therapy designed to reduce insulin resistance decreases concentrations in blood not only of insulin but also of PAI-1. Thus, the treatment of subjects with diabetes, and particularly type 2 diabetes, should focus not only on improved metabolic control but also on reduction of insulin resistance and hyperinsulinemia. Treatment designed to treat both the hormonal and metabolic abnormalities of diabetes is likely to reduce hyperactivity of platelets, decrease the intensity of the prothrombotic state, and normalize activity of the fibrinolytic system in blood and in vessel walls, thereby reducing the rate of progression of macrovascular disease and its complications. 2 tables. 114 references.

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Enteral vs. Parenteral Nutrition Support: Part One. Today's Dietitian. 3(8): 10-12. August 2001.

Advances in both enteral (through the digestive tract) and parenteral (outside the digestive tract) products and devices have made clinical nutrition a most exciting and rewarding area of practice. This article, the first of two in a continuing education series for dietitians, explores the pros and cons of parenteral support. Total parenteral nutrition (TPN) provides nutrients to a patient via vascular (blood vessel) access and can provide most of the necessary nutrients to patients unable to utilize their gastrointestinal (GI) tract effectively. Guidelines for the use of TPN include massive small bowel resection (surgical removal), severe diarrhea (if unresponsive to other treatments), intractable vomiting, acute pancreatitis, and malnutrition (if the patient is unable to use the GI tract for seven to 10 days). The authors describe access issues for TPN, formula preparation, fats, monitoring the TPN patient, and complications. Complications of TPN include phlebitis (inflammation of a vein) at the access site, pneumothorax (collapsed lung) during the insertion of the central line, thrombosis (clotting) of the vein, and infection of the venous access line. And because parenteral nutrition is much more complex and expensive than enteral nutrition therapies, its use must be closely monitored. 2 figures. 10 references.

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Hepatobiliary Diseases: Pathophysiology and Imaging. Malden, MA: Blackwell Science, Inc. 2001. 764 p.

This textbook aims to familiarize the reader with various imaging modalities, the information they provide, and with the merits of each, in order to facilitate the combined use of different imaging techniques in the diagnosis and management of hepatobiliary (liver and bile tract) diseases. The book includes 47 chapters in seven sections: progress in imaging, anatomy and gross changes in the liver, diffuse liver diseases, vascular disease, space-occupying lesions, other liver diseases, and biliary tract disease. Specific topics include computed tomography (CT scan) and magnetic resonance imaging (MRI); harmonic ultrasound; anatomy of the liver; acute hepatitis and acute hepatic failure; chronic hepatitis; cirrhosis (liver scarring); fatty liver (steatosis); alcoholic liver disease; iron overload; Wilson's disease; amyloidosis, metabolic diseases, drug-induced and chemical-induced liver injuries; vascular anatomy of the liver and vascular anomalies; portal hypertension (high blood pressure); thrombosis (clotting) affecting the liver; Budd-Chiari syndrome; primary malignant tumors of the liver (liver cancer); benign liver lesions; cysts of the liver; liver abscess; blunt hepatic trauma; parasitic diseases; infections and the liver; transplantation; anatomy of the biliary tract; congenital anomalies and dilatation; Caroli's disease; stone disease (gallstones); biliary tract stenosis; primary sclerosing cholangitis; cholecystitis and Mirizzi syndrome; tumors of the gallbladder; adenomyomatosis and cholesterolosis; Hilar carcinoma; and tumors of the common bile duct and papilla of Vater. Each chapter includes black and white reproductions of imaging techniques and a list of references. The book includes a color plate section and a detailed subject index.

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