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The factors that contribute to the achievement and maintenance of a healthy weight are essentially those acts and behaviors that can be considered a "healthy lifestyle medicine hat jobs purchase risperdal 4 mg line. Surgeon General recommends at least 30 minutes of moderate physical activity daily. This situation prevails despite the introduction and availability of dietetic, fat-free, low-fat, sugar-free and low-calorie foods and beverages, not to mention the pervasive presence of health clubs in most communities. Obesity has increased in every region of the United States, has affected both genders, and crosses all age groups, ethnicities, and education levels. Although the number of obese Americans stood at just 13% in 1962, two-thirds of Americans are now classified as overweight or obese (62% of women). This unfortunate "state of the weight" in the United States ultimately may undo the steady gains in overall health that Americans have enjoyed since the dawn of the 20th century. The food industry deserves its share of the blame, especially in the United States and most recently in Europe. Eating out more often with lack of portion control and inappropriate food choices, especially from fast food establishments, have all contributed to the obesity epidemic. The World Health Organization estimated in the year 2000 that as many as 300 million people worldwide were clinically obese. European countries are now following the health compromising trends found in the United States with as many as 30% of adults classified as overweight and obese. In the United States, the prevalence of obesity among Afro-Americans and those of Hispanic origin is higher than that of Caucasians. This change in physical play may be one of the explanations for the increased rates of obesity and type 2 diabetes in children. Once virtually unheard of in adolescence, type 2 diabetes now accounts for approximately half of all new diagnoses of diabetes in some populations. Overweight and obesity are both terms for ranges of weight that are greater than what is generally considered healthy for a given height and, as such, have been associated with an increased likelihood for adverse health consequences. The main stores for fat are subcutaneous and intra-abdominal; considerable amounts of fat can also reside within the muscles, especially in older adults. The gold standard for estimating body fat has been hydrodensitometry (underwater weighing), which is based on the principle that fat tissue is less dense than muscle and bone. Other methods used in assessing the amount of body fat are body circumference (waist and hip), that is, 40 in for men and >35 in for women are considered high; skinfold thickness and bioimpedance. Measurements of skinfold thickness can provide reasonable assessment especially if taken at multiple sites. Therefore, measurement of the resistance to a weak current (impedance) applied across the extremities, when combined with height and weight and an empirically derived equation, provides an estimate of body fat. It is a useful approximation of body fat, but it can often be misleading because muscular athletic individuals would most likely be considered overweight. However, regardless of the definition used, the adverse effects of excessive weight contribute to increased rates of perinatal mortality and morbidity. Heights and weights were self-reported during an interview and were then directly measured in a mobile examination site. The authors found that self-reported and measured height and weight were highly correlated. Unfortunately, many overweight and obese women are either not 260 the Diabetes in Pregnancy Dilemma cytokines have been reported to have paracrine as well as endocrine effects on many target tissues. Arteriosclerosis is now considered a disease of inflammation51 and serum concentrations of inflammatory markers have been demonstrated to be predictive of coronary events. They inhibit insulin action at the adipocyte and at the level of the hepatocyte and skeletal muscle by altering insulin receptor function. In turn, circulating inflammatory cells affect the endothelium and are a step in the development of atheromatous deposits. Therefore, obesity is also associated with an elevated risk of venous thromboembolic disease. They also influence liver and skeletal muscle that result in insulin resistance and dyslipidemia. This data corroborate that obesity in pregnancy is associated with metabolic, inflammatory, and vascular risk factors that may add to maternal complications in obese women. These metabolic and inflammatory stimuli induce microvascular dysfunction in preeclampsia and are proposed to arise from the placenta. The surplus inflammatory load that would occur as a result of obesity could potentially add fuel to this process, explaining at least in part the increased association of obesity with preeclampsia. Hypertension Disorders Hypertensive disorders have historically been associated with obesity in the pregnant and nonpregnant state. Authors have suggested a 10-fold higher rate of chronic hypertension in diabetic patients compared to normal-weight women. Very obese women were two to three times more likely to develop proteinuric preeclampsia. Birth weight above the 90th percentile also increased in very obese women as was the incidence of intrauterine death. Intrapartum complications included an increased rate of induction of labor and caesarean section delivery. In the postpartum period, there was an increased rate of hemorrhage, genital tract infection, urinary tract infection, and wound infection. They concluded that maternal obesity carries significant risk for both mother and fetus with risk increasing with the degree of obesity and persists after accounting for other confounding demographic factors. There was a 50% increase in frequency of fetal distress and twofold increase in cesarean delivery. Epidemiological studies have shown a relationship between pregnancies complicated by preeclampsia and increased risk of maternal coronary heart disease in later life. The reported increase in the relative risk of death from ischemic heart disease in association with a history of preeclampsia/eclampsia is approximately twofold. The metabolic syndrome explains the influence of obesity on the development of hypertensive disorders and ischemic heart disease, dyslipidemia, and coagulation abnormalities. A multitude of maternal, fetal, neonatal, and potentially lifelong complications increase significantly when partnered with obesity. These perinatal risks associated with maternal obesity stem from data obtained from a secondary analysis of a prospective cohort of >16,000 unselected patients in the United States. They speculated that the hyperlipidemia of obesity may reduce prostacyclin secretion and enhance peroxidase production, resulting in vasoconstriction and platelet aggregation thus affecting placental perfusion. In modern obstetrics with appropriate fetal surveillance testing and the recognition of the potential at risk status of the fetus of the obese patient, the majority of perinatal mortality cases can be prevented, leaving macrosomia as the main concern for these neonates. Maternal complications include hypertension, diabetes, respiratory complications, (asthma and sleep apnea), thromboembolic disease, more frequent cesarean delivery with increased wound infection, endometritis, and anesthetic complications (mainly difficulties in intubation and placement of epidural). Newborn complications include large-for-gestational-age infants, stillbirths, shoulder dystocia, and long-term complications (obesity and diabetes). A discussion of these complications should be the balance between the benefit/risk ratio of fetal and maternal perspectives. Abortion and Anomalies A meta-analysis of 13 studies examined patient predictors for outcome of gonadotropin ovulation induction. The study revealed that the best predictors of poor outcome are obesity and insulin resistance. The study demonstrated that obese women were approximately three times more likely than average-weight women to have an infant with either spinabifida or an omphalocele and about twice as likely to have a baby with either a heart defect or multiple anomalies, independent of intake of periconception multivitamins Table 23-2. Increasingly, maternal pregravid weight and decreased pregravid insulin sensitivity have been shown to strongly correlate with fetal growth, especially fat mass at birth. Low birth weight may be a significant variable for the development of the metabolic syndrome in adulthood.

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Every person with type 2 diabetes should receive diabetes education: they should learn about self-care symptoms electrolyte imbalance purchase line risperdal, self-monitoring of glucose at home, critical glucose values, what to do during sickness, and so forth. In the Diabetes Prevention Program, the subgroup receiving metformin had a 31% relative reduction in progression to type 2 diabetes at 2. At the end of two years, a 58% relative risk reduction for type 2 diabetes was reported in the women on troglitazone that persisted after a washout period of more than eight months. Pharmacological therapy in prediabetes appears encouraging, but not enough information is available to recommend it at present. Meal Plan Although in daily practice this is a very difficult task, patients should be encouraged to at least not gain weight. The latest recommendations from the American Diabetes Association are based mostly on expert opinion and data from single high-quality clinical trials and poorly controlled or uncontrolled studies. High-quality studies have not demonstrated benefit from routine supplementation with antioxidants such as vitamins E and C and carotene, and as their long-term safety is unknown these are not recommended. A summary of these can be found each year in the American Diabetes Association Clinical Practice Recommendations. Diabetes Self-Management Education and Support Education of patients regarding their diabetes is fundamental to care. Certified Diabetes Educators are available in most Depression Depression is common and should be screened for and treated with behavioral therapy and/or medication. Regular reassessment of diabetic control is essential to keep A1c within target values. Potential side effects of each drug must be discussed with the patient at the onset of therapy. Several different insulin formulations are available that differ in time of onset and duration of action. Treatment of Hypertension Hypertension should also be treated initially with lifestyle modification. All patients should be advised not to smoke and counseling, behavior modification techniques, and pharmacotherapy with nicotine or bupropion should be considered as therapy. Because these conditions are asymptomatic at onset, it is imperative for the health care professional to actively investigate for early metabolic abnormalities, to offer counseling with the assistance of other health care professionals, such as nutritionists and diabetic educators, and to extend these recommendations to the entire family. Bariatric Surgery Bariatric surgery is now recognized to be highly effective therapy for type 2 diabetes in many individuals. In addition to management of hyperglycemia, dyslipidemia, hypertension, and obesity should be aggressively managed to prevent micro- and macrovascular complications. Deaths, Percent of Total Deaths, and Death Rates for the 15 Leading Causes of Death in 5-Year Age Groups, by Race And Sex: United States, 2010; 2013. Impact of diabetes mellitus on life expectancy and health-adjusted life expectancy in Canada. Excess risk of fatal coronary heart disease associated with diabetes in men and women: meta-analysis of 37 prospective cohort studies. Drug therapy is indicated if, after a period of about three months, target values are not achieved. Muscle aches and cramps are reported in a small group of patients and occasionally the drug has to be discontinued. Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. Optimal medical therapy, lifestyle intervention, and secondary prevention strategies for cardiovascular event reduction in ischemic heart disease. Kahn R, Buse J, Ferrannini E, Stern M; American Diabetes Association, European Association for the Study of Diabetes. The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. The metabolic syndrome in overweight Hispanic youth and the role of insulin sensitivity. Metabolic and behavioral characteristics of metabolically obese but normal-weight women. Does inflammation determine whether obesity is metabolically healthy or unhealthy Targeting adipose tissue inflammation to treat the underlying basis of the metabolic complications of obesity. Does the metabolic syndrome improve identification of individuals at risk of type 2 diabetes and/or cardiovascular disease Energy balance and carcinogenesis: underlying pathways and targets for intervention. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United States. Nonalcoholic fatty liver disease and the metabolic syndrome: clinical implications and treatment. The effect of obesity on polycystic ovary syndrome: a systematic review and meta-analysis. Relation of functional ovarian hyperandrogenism to non-insulin dependent diabetes mellitus. Waist circumference and waist-to-hip ratio are related to gestational glucose tolerance. Incidence and risk factors associated with abnormal postpartum glucose tolerance in women with gestational diabetes. Follow-up study of 360 subjects with abnormal carbohydrate metabolism during pregnancy. Antepartum predictors of the development of type 2 diabetes in Latino women 11-26 months after pregnancies complicated by gestational diabetes. Gestational diabetes mellitus: the prevalence of glucose intolerance and diabetes mellitus in the first two months post partum. Prepregnancy weight and antepartum insulin secretion predict glucose tolerance five years after gestational diabetes mellitus. The experience at Los Angeles County/University of Southern California Medical Center. Gestational diabetes mellitus increases the risk of cardiovascular disease in women with a family history of type 2 diabetes. Increased risk of cardiovascular disease in young women following gestational diabetes mellitus. Gestational diabetes: the forerunner for the development of maternal and childhood obesity and metabolic syndrome Mild gestational hyperglycemia, the metabolic syndrome and adverse neonatal outcomes. Excessive obesity in offspring of Pima Indian women with diabetes during pregnancy. Perinatal hyperinsulinism and perinatal obesity as risk factors for hyperinsulinaemia in later life. Therapeutic management, delivery, and postpartum risk assessment and screening in gestational diabetes. Risk factors for type 2 diabetes among women with gestational diabetes: a systematic review. Racial and ethnic disparities in diabetes risk after gestational diabetes mellitus. Preservation of pancreatic beta-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk hispanic women. Pathophysiologic approach to therapy in patients with newly diagnosed type 2 diabetes. Pharmacogenetics in type 2 diabetes: potential implications for clinical practice. Therefore, the primary mission in screening for diabetes in general and gestational diabetes in particular justify the effort and cost of early identification in patients at risk for the disease. Even with identification, justification for screening will be determined if an intervention exists that decreases the adverse outcome with timely initiation. It is the leading cause of blindness in adults, kidney disease/failure, and most nontraumatic, lower extremity amputations. Those with diabetes are twice as susceptible to heart disease and two to six times more likely to have a stroke.

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Interface hepatitis treatment wasp stings cheap risperdal 2 mg overnight delivery, also known as piecemeal necrosis, refers to mononuclear inflammation extending from the limiting plate of the portal tract to envelop adjacent hepatocytes. The end stage of this process is cirrhosis, in which dense fibrous bands divide the liver into parenchymal nodules. Currently, liver biopsy is the gold standard for diagnosis, staging, and follow-up of chronic liver disease. However, liver biopsy has limitations, such as high costs, a false-negative rate of up to 24%, a sampling error rate ranging from 25% to 40%, and morbidity and fatality rates of 3% and 0. If steatohepatitis is present, diffuse fat deposition dominates the imaging findings. In cases with fulminant manifestations, imaging may assess the extent of necrosis and exclude complications of acute hepatitis, such as ascites and spontaneous hepatic rupture. Additionally, after the intravenous injection of contrast material, the liver parenchyma may enhance heterogeneously. Patchy areas of arterial phase hyperenhancement may be visible and superficially resemble the appearance of an infiltrative malignancy. A key distinguishing feature is that perfusional hyperenhancement resulting from acute inflammation fades to isoattenuation during the venous phases; by comparison, infiltrative malignancies tend to appear heterogeneous and washout during the venous phases. There are no specific sonographic findings in acute hepatitis, although hepatomegaly may be appreciated. Ultrasound is operator dependent, however, and these findings have limited reproducibility. Patients presenting with a clinical history of malaise, nausea, anorexia, fever, and right upper quadrant abdominal pain associated with jaundice and pruritus should be investigated promptly with liver function tests and an abdominal ultrasound evaluation. Other possible findings include nonspecific parenchymal heterogeneity, heterogeneous enhancement after intravenous contrast agent administration, and lymphadenopathy. Lymphadenopathy, in particular, is an important consideration because it is present in up to 65% of cases and may be the only indication of chronic active hepatitis in up to 35% of cases. In recent years, the rising prevalence of chronic hepatitis in Western nations has spurred the development of noninvasive, imagingbased techniques to assess parenchymal inflammation, hepatocellular injury, and liver fibrosis. A, Transverse ultrasound image shows nodular contours of the liver and a diffusely heterogeneous parenchymal echotexture. Note the innumerable hypointense regenerative nodules carpeting the liver diffusely. During the pre-cirrhotic stages of liver disease, heterogeneity of hepatic parenchyma may be seen after intravenous contrast agent administration; however, this finding is nonspecific and has not been shown to permit noninvasive staging of liver fibrosis. In particular, transient and shear wave ultrasound elastography have shown potential to identify liver fibrosis as early as the F2 stage, when treatment can be implemented before irreversible cirrhosis incurs (see Chapter 5). Ultrasound depicts a liver usually decreased in size with heterogeneous echotexture and is useful for assessing portal venous flow direction and waveforms. These causes include exposure to various toxins or toxin ingestion, metabolic disease, and autoimmune hepatitis. They are generally easily distinguishable by obtaining a complete history and evaluating copper studies, autoimmune markers, and viral hepatitis serologic studies. The clinical differential diagnosis of chronic hepatitis is similar to that of the various causes of cirrhosis. As with acute hepatitis, a careful history and evaluation of laboratory studies provides direction. Scaglione S, Kliethermes S, Cao G, et al: the epidemiology of cirrhosis in the United States: a population-based study. Gines P, Quintero E, Arroyo V, et al: Compensated cirrhosis: natural history and prognostic factors. Riggio O, Masini A, Efrate C, et al: Pharmacological prophylaxis of hepatic encephalopathy after transjugular intrahepatic portosystemic shunt: a randomized controlled study. Gines A, Escorsell A, Gines P, et al: Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites. Marti-Llahi M, Guevera M, Gines P: Hyponatremia in cirrhosis: clinical features and management. Montalto G, Cervello M, Giannitrapani L, et al: Epidemiology, risk factors, and natural history of hepatocellular carcinoma. Seguchi T, Akiyama Y, Itoh H, et al: Multiple hepatic peribiliary cysts with cirrhosis. Libbrecht L, Cassiman D, Verslype C, et al: Clinicopathological features of focal nodular hyperplasia-like nodules in 130 cirrhotic explant livers. Yoshida H, Shiratori Y, Moriyama M, et al: Interferon therapy reduces the risk for hepatocellular carcinoma: national surveillance program of cirrhotic and noncirrhotic patients with chronic hepatitis C in Japan. Ochs A, Rossle M, Haag K, et al: the transjugular intrahepatic portosystemic stent-shunt procedure for refractory ascites. These disorders uniquely manifest portal hypertension before overt hepatic parenchymal disease and dysfunction, in contrast to other causes of hepatic disease in which hepatic dysfunction precedes portal hypertension. It also can result from extrinsic compression by malignant and benign solid tumors of the liver or adjacent organs, intrahepatic hematomas, hepatic abscesses, hydatid cysts, and hepatic cysts in polycystic kidney disease. The injured endothelial cells undergo a morphologic transformation from their normal spindle shape to a rounder configuration, which narrows the sinusoidal lumen and introduces gaps between the cells. Blood flows through the gaps into the space of Disse, detaching endothelial as well as other perisinusoidal cells. The detached cells embolize downstream, causing further sinusoidal and possibly venular obstruction. Eventually, sinusoidal and centrilobular fibrosis ensues, causing hepatic congestion and manifesting clinically as portal hypertension. Later, the resulting low-flow state causes redistribution of the hepatic microcirculation and focal hepatic ischemia, culminating in centrilobular hepatocyte necrosis. Increased sinusoidal pressure promotes centrilobular sinusoidal dilatation and congestion. Sinusoidal perfusion diminishes, and centrilobular ischemia and necrosis may occur. Areas in which there is simultaneous obstruction of the hepatic and portal veins undergo infarction. Large-scale epidemiologic studies to assess prevalence, incidence, and demographic factors have not been conducted. Serum values of aminotransferases, alkaline phosphatase, and bilirubin are moderately elevated, whereas those of plasma coagulation factors are diminished. The presentation is chronic in 80% of patients; 20% of these patients progress to cirrhosis. In both conditions, acute venous obstruction is characterized by dilated centrilobular sinusoids filled with erythrocytes. Associated findings include parenchymal compression as well as atrophy and loss of hepatocytes. Erythrocytes may extravasate into the space of Disse and replace the disappearing hepatocytes. In severe cases, blood-filled lakes may form in the centrilobular zone, with little recognizable hepatic parenchyma. Hemosiderinladen macrophages may be present, but inflammation is absent to minimal. This form of fibrosis spares the portal tracts, resulting in a pattern termed reserve lobulation or venocentric cirrhosis, although end-stage cases may be indistinguishable from cirrhosis from other causes. The first symptom is abdominal pain, followed by ascites, tender hepatomegaly, jaundice, and weight gain (from fluid retention). Laboratory abnormalities include direct hyperbilirubinemia initially with subsequent elevations in alkaline phosphatase and aminotransferases. Renal dysfunction (with up to 50% of patients requiring dialysis), diuretic-resistant fluid retention, recalcitrant thrombocytopenia resulting from splenic sequestration, and encephalopathy occur later. Both sets of criteria use variable combinations of hyperbilirubinemia, weight gain, ascites, and hepatomegaly within 3 weeks of stem cell transplantation. If percutaneous biopsy is contraindicated because of thrombocytopenia, a transjugular approach may be employed, at which time the hepatic venous pressure gradient may also be measured. When elevated above 10 mm Hg, this gradient has a specificity of 90% in the appropriate clinical scenario.

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In patients with bowel obstruction or gastroenteritis there is increased peristaltic activity and also a large amount of luminal fluid that makes the examination much easier to interpret treatment 3rd degree av block order risperdal 4mg on line. The valvulae conniventes (arrows) are well demonstrated projecting into the fluid-filled small bowel. Labeled leukocyte imaging is a noninvasive technique for the detection of occult inflammation and infection. Because leukocytes can be separated and labeled without significant loss of function, they can be used to image small bowel inflammation and disease complications, such as abscess and possibly fistula. Adjacent to the thickened bowel are slightly enlarged mesenteric lymph nodes showing hyperemia on color Doppler imaging (arrowheads). Several studies have examined the role of labeled leukocyte scintigraphy in the assessment of disease extent in patients with established inflammatory bowel disease. Another advantage includes evaluation of the entire small and large bowel at the same time. The technique has the potential for verifying the presence of intraabdominal and extraabdominal abscesses and, possibly, fistulas. Pros and Cons Because of its low specificity, this technique may not be able to distinguish between infective enteritis and inflammatory or ischemic bowel conditions. Also, activity within the abdomen may be due to causes other than inflammation and has the potential for misinterpretation. Rarely, complications such as bleeding, intussusception, ulceration, obstruction, or torsion can occur. Principle the principle of 99mTc-pertechnetate scintigraphy is that the pertechnetate anion is selectively taken up by the surface mucussecreting cells that line the gastric mucosa whether it is located in the stomach or is ectopic. Pertechnetate scintigraphy has a sensitivity of 80% to 90%, a specificity of 95%, and an accuracy of 90% in children. Radionuclide studies have typically been used as a screening examination to identify patients who require targeted angiography or surgery. Lower gastrointestinal tract bleeding is more frequent in the colon as opposed to the small bowel. The most common causes of colonic bleeding include mucosal vascular malformations such as angiodysplasia, diverticulum, adenomatous neoplasms, and polyps. Colonoscopy performed within 24 hours of hospital admission will confirm a colonic bleeding site in 68% to 77% of cases. Angiography will locate gastrointestinal bleeding sites in up to 65% of cases when hemorrhage occurs at a rate greater than 1 mL/min. The majority of gastrointestinal bleeding, however, is intermittent, and bleeding may not be occurring during contrast injection (20 to 30 seconds). A, Select anterior image shows abnormal activity left of the midline in the lower abdomen (white arrow), appearing in the same temporal fashion as the stomach (black arrow). Physiologic activity is seen in the urinary bladder (arrowhead) and genitalia (arrow). Activity is also seen in the genitalia, and there is some urinary excretion of free pertechnetate. Gastrointestinal hemorrhage appears as a focal activity, not in the expected location of blood pool or urinary excretion. Endoscopy of the upper gastrointestinal tract is reported to have an overall diagnostic accuracy of more than 90% in identifying duodenal and gastric ulcers, gastric erosions, varices, and Mallory-Weiss tears. Somatostatin is a neuropeptide that is secreted and released by endocrine and nerve cells, especially by the hypothalamus. Somatostatin inhibits the release of growth hormone, insulin, glucagon, gastrin, serotonin, and calcitonin. Because carcinoid tumor is of neuroendocrine origin, a high density of somatostatin receptors is present. Image Interpretation In a normal scintiscan the activity is identified in the blood pool, thyroid gland, liver, gallbladder, spleen, kidneys, and bladder. As the somatostatin is excreted by the kidneys, significant activity is seen in the kidneys on the delayed images. Tumor is seen as a focal area of increased uptake that persists on the delayed scintiscans. Octreotide scintigraphy serves as an efficient screening tool in patients with suspected carcinoid. However, an abnormal focus of activity is seen in the right lower quadrant (arrow) and in the mesentery in the midline (arrowhead). B, Computed tomography scan in the same patient in the mid-abdomen demonstrating thickening of the terminal ileum (arrow) and an adjacent lymph node. Long segments of abnormal bowel are easy to see as long as frequent fluoroscopy is performed. The small bowel folds are also better evaluated by enteroclysis because the folds are straightened. Inadequate distention can mask subtle areas of bowel wall thickening or may falsely mimic wall thickening. These sequences limit respiratory and motion artifact and provide excellent-quality images. Inflammation and infection evaluation detects intraabdominal and extraabdominal clinically occult inflammation and infection. In neoplasm evaluation, octreotide scintigraphy has an 85% to 95% sensitivity for carcinoids. Gourtsoyiannis N, Papanikolaou N: Magnetic resonance enteroclysis of the small bowel. Rosch T, Classen M: Gastroenterologic endosonography, New York, 1992, Thieme Medical Publishers, p 36. Fever, hypotension, tachycardia, and leukocytosis are suggestive of strangulation. Bowel sounds can be hyperactive in an early stage of obstruction or hypoactive late in the course as well as with strangulated lesions. Peritonitis and perforation present as a silent tender abdomen and are late signs. It measures approximately 120 cm in length from the pylorus to the ileocecal valve. The potential surface area available for digestion is increased approximately 600 times by the presence of the circular folds, villous mucosa, and microvillar surface of the epithelium. The jejunum and ileum receive their blood supply from the superior mesenteric artery and its vascular arcades. Venous drainage is by the superior mesenteric vein, which joins the splenic vein posterior to the pancreas to form the portal vein. Small bowel loops are suspended by a mobile mesentery and covered by a lining of peritoneum that extends over the serosal surface of the bowel. Lymphatic drainage of the small bowel is into the regional lymph nodes, which follow the vascular arcades and drain into the cisterna chili. Loops of jejunum are mostly located in the left hypochondrium in an individual with normal gut rotation. Knowing the normal bowel gas pattern on abdominal radiographs is important because this determines the ability to detect deviation from the normal pattern and classify this further. This bowel dilatation stimulates cell secretory activity, resulting in more fluid accumulation. This leads to increased peristalsis both above and below the obstruction with frequent loose stools and flatus early in its course. This can cause compression of mucosal lymphatics, leading to bowel wall lymphedema. Mortality decreases to 8% if surgery is performed within 36 hours and to 25% if the surgery is postponed beyond 36 hours. Colicky pain is more often associated in patients with simple obstruction and increases in severity.

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Although time consuming and invasive medications januvia buy risperdal 3 mg fast delivery, it can enable therapeutic intervention through thromboaspiration, thrombolysis, and vasodilator therapy. Patients suspected of having nonocclusive mesenteric ischemia should be promptly referred for angiography. Angiography is recommended in clinically suspected nonocclusive mesenteric ischemia Table 26-4). Classic Signs: Nonocclusive Mesenteric Ischemia Nonocclusive Mesenteric Ischemia Except for the absence of occlusive lesion within visceral arteries, the radiologic features of nonocclusive mesenteric ischemia may be identical to other forms of acute mesenteric ischemia. Bowel wall that uniformly enhances greater than venous enhancement may be seen in shock bowel-a form of nonocclusive mesenteric ischemia seen in hypotensive and hypovolemic patients. There is no role for ultrasonography in the assessment of nonocclusive mesenteric ischemia. There is no role for scintigraphy in the evaluation of nonocclusive mesenteric ischemia. Duplex ultrasonography may be useful in assessing mesenteric venous thrombosis by demonstrating a lack of portomesenteric blood flow and intraluminal echogenic debris. However, evaluation is limited by bowel gas, patient body habitus, and patient noncooperation. Collateral vessels may be incompletely imaged or may be mistaken for patent central veins. There is no role for scintigraphy in the evaluation of mesenteric venous thrombosis. Mesenteric venous thrombosis may be evaluated angiographically by direct portography, such as transhepatic or transjugular portography or splenoportography. Such techniques also provide an avenue for endovascular intervention such as angioplasty. B, Multiple loops of small bowel demonstrate wall thickening (arrow) with adjacent hazy attenuation of mesentery (arrowheads) consistent with venous congestion. The superior mesenteric artery demonstrates vascular calcifications, which are partially obscured by intraluminal contrast. A high index of suspicion is needed to facilitate early diagnosis and intervention and should be prompted when peritoneal signs are present. Clinicians may consider acute inflammatory disorders such as pancreatitis, cholecystitis, or inflammatory bowel disease, although pain may be more localized compared with acute mesenteric ischemia. Acute mesenteric ischemia should be considered strongly in patients with prior embolic events or cardiac disease or who are critically ill or are on vasopressor therapy. Patients with a primary clotting disorder may prompt consideration of mesenteric venous thrombosis. Pneumatosis intestinalis is more specific for ischemia, although infection and trauma are other possible causes. Portal-to-portal and portal-to-system collateral vessels may also be demonstrated. B, Delayed venous phase of the arteriogram demonstrates nonopacification of the superior mesenteric vein and its tributaries, consistent with thrombosis. Diffuse mesenteric arterial narrowing on angiography without evidence of occlusion suggests nonocclusive mesenteric ischemia, although vasculitis also may be considered. Filling defects within mesenteric veins are diagnostic of mesenteric venous thrombosis and are often easily distinguished from extrinsic compression by tumor such as by pancreatic malignancy. Medical therapy should begin with fluid resuscitation and, if there is no contraindication, anticoagulation. Similarly, mesenteric venous thrombosis may be treated medically unless there is evidence of bowel infarction, in which case laparotomy is mandated. Anticoagulation is the mainstay of therapy, and some patients recover spontaneously. Because vasospasm of otherwise unaffected mesenteric vessels may occur after revascularization, angiography and intraarterial catheter infusion of a vasodilator such as papaverine may be performed before surgery unless reperfusion is established within 3 hours of onset. If, however, a bypass graft is necessary to augment flow after thrombectomy, the arteriotomy site may serve as the distal anastomosis. Autologous vein grafts are mandated when there is intraperitoneal contamination from bowel perforation. Thrombectomy is sometimes employed in cases of focal, acute mesenteric venous thrombosis within the proximal superior mesenteric vein. Further studies are required comparing percutaneous with surgical revascularization. Intraarterial vasodilator therapy may be helpful in acute mesenteric ischemia to prevent or treat vasospasm. Please refer to the discussion of mesenteric vessel anatomy in the previous chapter on acute small bowel ischemia. In rare cases, only one vessel is involved and distal disease predominates, thus circumventing proximal collateral flow. The postprandial nature of the Chronic Small Bowel Ischemia Atherosclerotic disease is the primary cause of chronic mesenteric ischemia, accounting for more than 95% of cases. A severe stenosis is also demonstrated at the origin of the superior mesenteric artery (arrow). Loss of signal at the celiac artery (arrowhead) and origin of the superior mesenteric artery (long arrow) is consistent with severe stenosis. Because most patients with mesenteric vascular disease are asymptomatic, its presence is not diagnostic of chronic mesenteric ischemia. In the setting of severe stenosis or occlusion of at least two mesenteric vessels, the diagnosis may be suggested by clinical findings in the absence of evidence of an alternative pathologic process. Radiography Plain radiography is insensitive and nonspecific and is relegated to excluding other disorders, such as small bowel obstruction. A lateral abdominal radiograph may show calcified plaques at the origins of the mesenteric arteries. Findings of bowel wall thickening, target sign, pneumatosis, and portomesenteric gas indicate an acute process and are absent in chronic mesenteric ischemia. Limitations include susceptibility artifact from stents or poor demonstration of calcifications, with potential overestimation of severity of arterial stenoses. Increased oxygen extraction reduces oxygen saturation and, consequently, the T2 value of the blood in the superior mesenteric vein. A peak systolic velocity of greater than 275 cm/s correlates with a stenosis of at least 70%,3,21 whereas lack of flow is consistent with occlusion. In addition, sonographic evidence of stenosis may suggest atherosclerotic disease but does not necessarily imply chronic mesenteric ischemia. Evaluation of the inferior mesenteric artery as well as more distal portions of the mesenteric vessels is limited. Nuclear Medicine There is no role for scintigraphy in the evaluation of chronic mesenteric ischemia. Angiography Angiography is the gold standard in evaluating the mesenteric vasculature. Anteroposterior aortography and selective mesenteric angiography are used to assess distal disease as well as to demonstrate collateral vessels. New-onset or recent worsening of symptoms should prompt evaluation for acute mesenteric ischemia. Postprandial pain can be seen with gastroduodenal ulcers, which should be excluded by endoscopy. Weight loss is a nonspecific complaint that should prompt evaluation for malignancy. Similarly, the finding in young female patients of abdominal pain and a history of hypertension may suggest fibromuscular dysplasia. Angiographic demonstration of extrinsic narrowing of the celiac origin that worsens with expiration is compatible with median arcuate ligament syndrome. Surgery has high long-term patency rates (70% to 93%) but may be associated with a morbidity of 29% and mortality of 7%,28 with complication rates exacerbated by cardiovascular comorbidities, which are common in this patient population. Although further studies are required, angioplasty and stenting have high technical success rates; restenoses may be re-treated percutaneously. Percutaneous revascularization may be preferred in patients who are high-risk surgical candidates.

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A comparison between the minimal model and the glucose clamp in the assessment of insulin sensitivity across the spectrum of glucose tolerance 2c19 medications buy cheap risperdal 3 mg on line. Insulin sensitivity and -cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes. Tumor necrosis factor impairs insulin action on peripheral glucose disposal and hepatic glucose output. Multiple metabolic defects during late pregnancy in women at high risk for type 2 diabetes. Islet cell antibodies identify a subset of gestational diabetic women with higher risk of developing diabetes shortly after pregnancy. Incidence and significance of islet cell antibodies in women with previous gestational diabetes. Molecular mechanisms and clinical patho-physiology of maturity-onset diabetes of the young. High prevalence of a missense mutation of the glucokinase gene in gestational diabetic patients due to a founder-effect in a local population. Pronounced insulin resistance and inadequate -cell secretion characterize lean gestational diabetes during and after pregnancy. Subclinical abnormalities of glucose metabolism in subjects with previous gestational diabetes. Defects in insulin secretion and action in women with a history of gestational diabetes. Insulin receptor binding and tyrosine kinase activity in skeletal muscle from normal pregnant women and women with gestational diabetes. Phosphatidylinositol 3-kinase redistribution is associated with skeletal muscle insulin resistance in gestational diabetes mellitus. Impaired glucose transport and insulin receptor tyrosine phosphorylation in skeletal muscle from obese women with gestational diabetes. Multiple defects in the adipocyte glucose transport system cause cellular insulin resistance in gestational diabetes. Calpain-10 haplotype combination and association with gestational diabetes mellitus. Sulfonylurea receptor 1 gene variants are associated with gestational diabetes and type 2 diabetes but not with altered secretion of insulin. Differential regulation of genes for fetoplacental lipid pathways in pregnancy with gestational diabetes and type 1 diabetes mellitus. History of gestational diabetes leads to distinct metabolic alterations in nondiabetic AfricanAmerican women with a parental history of type 2 diabetes. Gestational diabetes mellitus: the prevalence of glucose intolerance and diabetes mellitus in the first two months postpartum. Long-term diabetogenic effect of a single pregnancy in women with prior gestational diabetes mellitus. Changes in insulin secretion and sensitivity during the development of type 2 diabetes after gestational diabetes in Hispanic women. Preservation of pancreatic B-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk hispanic women. Prevention of diabetes in women with a history of gestational diabetes: effects of metformin and lifestyle interventions. Opinions and anecdotes have been more prolific than research generated data on this issue. In a letter to the editor, Hunter and Milner stated that "gestational diabetes is a diagnosis still looking for a disease. Lack of agreement on universal screening, diagnostic criteria, and the methodology for glucose tolerance testing led to inconsistency in the results of published studies. The definition applies regardless of treatment modality and/or the persistence of the condition after pregnancy when it will be termed type 2 diabetes when indicated. Both assumptions had the potential to either decrease cost of care when treatment is not warranted or enhance quality of care by decreasing morbidity. These alterations in insulin have been previously ascribed to a variety of reproductive hormones such as human placental lactogen, cortisol, progesterone, and estrogen. Whatever the cause for increased insulin resistance during pregnancy, in women who maintain normal glucose tolerance, it is offset by a 3- to 3. Some stressors associated with pregnancy probably trigger them to develop overt disease sooner than if they had not become pregnant. It generally recurs with subsequent pregnancies and is clearly the harbinger of abnormal glucose metabolism in later life. They probably have some degree of insulin resistance prior to pregnancy and normal pregnancy is associated with severe insulin resistance. For instance, targeting the desired level of glycemia with the appropriate treatment modality and control of weight gain may positively affect the rate of macrosomia, metabolic and respiratory complications, and so on. The unmodifiable variables will include maternal age, ethnicity, obesity, and genetic factors. Furthermore, certain outcome variables will be influenced by physician behavior based on legal and social pressures. Research studies need to report outcome variables both as univariant data and as multivariant analysis to show the net effect of each variable; this process controls for confounding effects. Composite outcomes that combine several specific outcomes are often used as primary outcomes in obstetric studies. It is advantageous to use composite outcomes as they make trial designs more efficient. The most frequently cited reason for using composite outcome is that of statistical efficiency. Even though the whole is equal to the sum of its parts, not all the parts carry equal weight. Each component should be presented as a secondary outcome so that readers can make up their own minds about the relevance of each outcome in the overall rate. Therefore, the reported rate of a composite outcome is affected by the outcome variables that have been selected for inclusion. Thus, the use of a composite outcome does not always lead to an increase in the evidence supporting a benefit for an intervention. Until standardized methods are available, researchers who decide to use a composite outcome in a clinical trial should carefully consider the rationale for selecting each component outcome for short- and long-term consequences. However, after age 5, there is a rapid weight gain and by age 8, almost half of the offspring of diabetic mothers weigh at or above the 90 percentile. Adiposity in children is strongly correlated with childhood hypertension (both systolic and diastolic) and resembles the metabolic syndrome albeit in evidence at a younger age. The mean postprandial glucose value for the second and third trimester correlated with waist circumference (r = 0. The Brazelton scale has gained wide acceptance as one of the premier instruments for integrative characterization of nervous system function in the newborn period. In each case, poor glycemic control was followed by poorer Brazelton ratings of the neonate. The results were neither different when gestational diabetic and pregestational diabetics were analyzed separately nor could they attribute them to various prenatal events such as asphyxia, neonatal hypoglycemia, or differences in socioeconomic status or ethnicity. Although the authors reported that their patients were well controlled, this statement is questionable as there was an approximate 30% rate of macrosomia (>4000 g), hypoglycemia, and hyperbilirubinemia. On the other hand, this perinatal outcome demonstrated the long-term complications one can anticipate when the level of glycemia is uncontrolled. Maternal diabetes during pregnancy may affect behavioral and intellectual development in the offspring.

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Adequate fluid intake is therefore important to the action of bulk-forming laxatives symptoms toxic shock syndrome purchase 4 mg risperdal visa. This can be useful for some patients with diverticular disease, irritable bowel syndrome, or when managing stoma output. These drugs are generally well tolerated, with mild abdominal distension and flatulence being the most common side effects. Rarely, but more seriously, they may cause faecal impaction and gastrointestinal obstruction. They should not be used in patients with subacute or established intestinal obstruction or faecal impaction, and in general should not be used in patients with ileus. There are no clinically significant adverse drug interactions with bulk-forming laxatives. Bulk-forming laxatives may be provided in the form of granules or powder to be dissolved in water (ispaghula husk, sterculia) or tablets (methylcellulose). Tell them that the dose can be adjusted according to their symptoms, provided they do not exceed the maximum dose. Patients who need to pay for their prescription may save money if they buy it from a pharmacy. Administration Communication Monitoring Cost Clinical tip-Do not routinely use bulk-forming laxatives for patients with new-onset constipation who have recently had abdominal surgery and may have surgical (paralytic) ileus, as they will be at increased risk of developing intestinal obstruction. These medicines are based on osmotically active substances (sugars or alcohols) that are not digested or absorbed, and which therefore remain in the gut lumen. It does this by increasing gut transit rate and acidifying the stool, which inhibits the proliferation of ammoniaproducing bacteria. This is helpful in patients with liver failure, in whom ammonia plays a major role in the pathogenesis of hepatic encephalopathy. Flatulence, abdominal cramps and nausea are common adverse effects, although they may decrease with time. Osmotic laxatives are contraindicated in intestinal obstruction as there is a risk of perforation. Phosphate enemas can cause significant fluid shifts so should be used with caution in heart failure, ascites and when electrolyte disturbances are present. There are no significant adverse drug interactions with osmotic laxatives, although the effects of warfarin may be slightly increased. For example, when treating constipation or faecal impaction you might prescribe lactulose 15 mL twice daily, titrating this to response. Be aware that it may take a few days for an effect to be seen, as the drug needs to pass through the gastrointestinal tract to the colon. When using a phosphate enema to treat faecal impaction, prescribe it in the once-only or as-required section for rectal administration. For bowel preparation, you should refer to a local protocol for prescribing advice. Oral solutions can be taken as they are or diluted in another liquid; powdered forms are dissolved in water. Enemas are administered with the patient lying on their side, as for a rectal examination. They should stay in this position for a few minutes or until they need to open their bowels. Explain that you are offering treatment with a laxative that will hopefully make their stool softer and easier to pass. If they are regularly passing more than two or three soft stools per day, the dose should definitely be reduced or the laxative stopped (unless being used for hepatic encephalopathy). When treating inpatients, a stool chart is useful to monitor the effects of treatment. This is particularly important when treating hepatic encephalopathy, where you should also monitor electrolytes. Administration Communication Monitoring Cost Clinical tip-When treating faecal impaction with rectally administered laxatives, try a glycerol suppository (stimulant laxative) before using a phosphate enema. Phosphate enemas are irritant and are administered as a significant volume of fluid (>100 mL), which can be quite uncomfortable when administered. Stimulant (also known as irritant or contact) laxatives increase water and electrolyte secretion from the colonic mucosa, thereby increasing volume of colonic content and stimulating peristalsis. They also have a direct pro-peristaltic action, although the exact mechanism differs between agents. For example, bacterial metabolism of senna in the intestine produces metabolites that have a direct action on the enteric nervous system, stimulating peristalsis. Rectal administration of stimulant laxatives, such as glycerol suppositories, provokes a similar but more localised effect and can be useful to treat faecal impaction. Abdominal pain or cramping may occur with stimulant laxative use and diarrhoea is an obvious potential adverse effect. With prolonged use, some stimulant laxatives cause melanosis coli (reversible pigmentation of the intestinal wall). Stimulant laxatives should not be used in patients in whom intestinal obstruction is suspected as there is a risk that this could induce perforation. Rectal preparations are usually avoided if haemorrhoids or anal fissure are present. There are no clinically significant adverse drug interactions with stimulant laxatives. When treating faecal impaction, rectal stimulant laxatives should usually be prescribed once only or as required with a maximum dose frequency of once in a 24-hour period. Stimulant laxatives are usually administered orally, unless treating faecal impaction when glycerol suppositories may be administered rectally. Explain that you are offering treatment with a laxative that will help stool to pass. Advise your patient that stimulant laxatives do not work immediately and they may need a few doses before a sustained effect is noticed. If they are regularly passing more than two or three soft stools per day, the dose should definitely be reduced or the laxative stopped. Mention that side effects such as abdominal cramps and flatulence can occur, but these may get better over time. Patients who pay for their prescriptions may save money if they buy them over the counter. Administration Communication Monitoring Cost Clinical tip-When prescribing opioid analgesics to be taken regularly, consider co-prescribing a laxative to prevent constipation. Patients find constipation uncomfortable and it can contribute to confusion in the elderly, so prevention can increase adherence to opioid treatment and control of symptoms. Lidocaine (formerly known as lignocaine) enters cells in its uncharged form, then accepts a proton to become positively charged. From inside the cell, it enters and then blocks voltage-gated sodium channels on the surface membrane. This prevents initiation and propagation of action potentials in nerves and muscle, inducing local anaesthesia in the area supplied by blocked nerve fibres. In the heart, it reduces the duration of the action potential, slows conduction velocity and increases the refractory period. The most common side effect is an initial stinging sensation during local administration. Systemic adverse effects are, predictably, more likely after systemic administration, whether intentional (as when it is used as an antiarrhythmic) or inadvertent (due to accidental intravascular injection during local administration). Its effects on the neurological system include drowsiness, restlessness, tremor and fits. It generally causes relatively little cardiovascular toxicity, but in overdose it may cause hypotension and arrhythmias. As the duration of action of local anaesthetics depends on how long they stay in contact with the neurones, co-administration with a vasoconstrictor.

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Splenomegaly may be the only finding of splenic hamartomas on plain radiography medicine wheel teachings risperdal 4 mg amex, when they are large enough to be visualized. Splenic hamartomas generally exhibit mildly low-signal to iso-signal intensity and moderately high signal intensity on T1- and T2-weighted images, but they may show heterogeneous signal intensity partly because of the varying-sized cystic spaces. If the amount of fibrous tissue is substantial, hamartomas may have regions of low signal intensity on T2-weighted images. A, Axial contrast-enhanced computed tomography scan during the arterial phase shows a heterogeneously enhancing mass (arrow) in the anterior pole of the spleen. B, On delayed phase, this lesion (arrow) shows as an isoattenuated to slightly hyperattenuated mass. C, the lesion is seen as a hypoechoic mass (arrow) on an oblique coronal ultrasound image. The cut surface of the specimen reveals a well-circumscribed, dark-red solid nodular lesion (arrows). A, Axial contrast-enhanced computed tomography scan shows an isoattenuation mass (arrows) in the spleen, which is not discriminated from the surrounding spleen. B, the ultrasonogram reveals a hypoechoic solid mass (arrows) with a well-defined margin. Axial T1-weighted (A), T2-weighted (B), early contrast-enhanced (C), and late contrast-enhanced (D) magnetic resonance images show a round splenic lesion (arrows) with iso-signal to slightly low signal intensity on T1- and T2-weighted images (A and B), heterogeneous character, good enhancement on arterial phase image (C), and more uniform enhancement on the portal phase image (D) the patient underwent ultrasonography-guided biopsy. Although the typical hypervascularity of the red pulp within the hamartoma may produce several angiographic findings, such as tumor vessels with aneurysmal dilatation, arteriovenous shunts, vascular lakes, and tumor blush, this examination is seldom performed for diagnostic purposes currently because of the advances in noninvasive imaging methods. Others have proposed a unified concept of lymphangioma and cystic hygroma as being a congenital developmental defect. Prevalence and Epidemiology Splenic lymphangioma is a relatively rare benign tumor with various clinical manifestations that range from an asymptomatic incidental lesion to a large symptomatic mass requiring surgery. Most splenic lymphangiomas occur in children, and adult cases are reported less frequently. A, Axial contrast-enhanced computed tomography scan shows a thin-walled, multilocular cystic mass with sharply demarcated margin in the anterior pole of the spleen. The cut surface of the gross specimen shows a multilocular cystic mass with thick fibrous walls and trabeculae. Lymphangiomas are either solitary or multiple or may replace the spleen in a condition called lymphangiomatosis. Clinical Presentation In patients with splenic lymphangiomas there is a close relationship between the occurrence of symptoms and splenic size. Larger lesions cause symptoms such as left upper quadrant pain, nausea, and abdominal distention. More extensive or larger lymphangiomas of the spleen may be complicated by bleeding, consumptive coagulopathy, hypersplenism, and portal hypertension. They often involve the capsule and trabeculae of the spleen, where lymphatics are normally concentrated, in contrast to the random localization seen with hemangiomas. Of the solitary subcapsular focal lesions, lymphangioma is the most common, when focal splenic infarction is excluded. With larger multifocal lesions, the tumors are separated by distinct residual splenic tissue. Lymphangiomas can be divided into three types according to the size of the vascular channels: capillary, cavernous, and cystic. The cut surface of the gross specimen shows numerous small foci of lymphangiomatous lesions disseminated throughout the spleen. Microscopically, these tumors consist of a single layer of flattened endothelium-lined spaces, filled with eosinophilic proteinaceous material instead of blood as seen in hemangiomas. Splenomegaly may be the only finding of splenic lymphangiomas on plain radiography, when they are large enough. However, the T1 signal intensity may be high, resulting from internal bleeding or the presence of large amounts of intracystic proteinaceous content. On ultrasonography, splenic lymphangiomas appear as well-defined anechoic cystic lesions with occasional internal septations and intralocular echogenic debris. Color Doppler ultrasonography can demonstrate the vasculature along the cyst walls. Nuclear medicine currently has no role in the evaluation of splenic lymphangiomas. Prevalence and Epidemiology Littoral cell angiomas may occur at any age and have no gender predilection. Although these tumors were originally thought to be benign, their biologic behavior has not been firmly established because there have been several reports of littoral cell angioma with malignant features. Also, an association between littoral cell angioma and other malignancies, including colorectal, renal, and pancreatic adenocarcinoma and meningioma, has been described. Other systemic symptoms such as fever, chills, weakness, fatigue, and pain have been reported. In most patients, splenectomy is performed because symptomatic hematologic problems are present and the imaging findings are nonspecific. Pathology Littoral cell angioma is a neoplasm with characteristic morphologic and immunophenotypic features distinguished from the other vascular splenic tumors. However, on delayed phase contrast-enhanced images, littoral cell angiomas homogeneously enhance and become isoattenuating relative to the remaining splenic parenchyma, a finding that may help limit the differential diagnosis. There is no significant abdominal adenopathy, which is typically seen in patients with splenic metastasis and lymphoma, in patients with littoral cell angioma. It has been speculated that this lesion represents a reactive tumor-like condition secondary to the infectious or autoimmune disorder. However, now this lesion generally is considered neoplastic and has been redesignated as myofibroblastic tumor. Although it is rare and generally considered benign, it is potentially a locally aggressive lesion. Microscopically, the lesion consists of inflammatory (lymphocytes, plasma cells, eosinophils, and histocytes) and spindle cells with varying amounts of granulomatous reaction, fibrosis, and necrosis. The predominant growth pattern may be sclerotic, xanthogranulomatous, or plasma cell granuloma type. Central coagulation necrosis is frequently seen, in association with a neutrophilic infiltration. Myofibroblastic tumors are seen as slightly hypointense and slightly hyperintense lesions compared with background spleen on T1- and T2-weighted images. Differential Diagnosis Many of the benign splenic tumors are incidentally found on imaging studies in asymptomatic patients or those with nonspecific symptoms. Because the most important aspect in the diagnosis of benign splenic tumors is the differentiation of the lesions from the more ominous abnormalities such as lymphoma and metastasis, careful physical examination is warranted to search for the palpable lymphadenopathy in the abdomen and other regions. Benign splenic tumors may be confidently diagnosed when they have typical findings on radiologic multimodalities studies. When a noninvasive diagnosis of benign splenic tumor is confident in asymptomatic patients, they may be safely observed without treatment. A, Axial contrast-enhanced computed tomography scan during the arterial phase shows a relatively well-defined solitary mass with heterogeneous hypoattenuation in the spleen. B, On delayed phase imaging, this mass becomes more isodense relative to the normal spleen. The cut surface of the gross specimen shows a well-defined solitary mass having a heterogeneous internal compartment, including fibrotic and hemorrhagic foci. Splenectomy may be indicated for the treatment of benign splenic tumors when a diagnosis is uncertain and other ominous splenic abnormalities cannot be excluded, when a biological behavior of the lesion is uncertain, and when patients are symptomatic. The histologic features of splenic angiosarcomas are similar to those of angiosarcomas in other locations. Microscopically, the tumor consists of disorganized anastomosing vascular channels lined by atypical endothelial cells with a high mitotic rate. Immunohistochemically, the tumor cells exhibit endothelial markers and frequently histiocytic markers as well. Imaging On cross-sectional imaging studies, angiosarcomas appear as either solitary or multiple nodular masses in an enlarged spleen, composed of a heterogeneous compartment including the area of hemorrhage or necrotic degeneration (see Table 59-2). In cases of spontaneous rupture, intraperitoneal hemorrhage will appear hyperattenuating on unenhanced images in the intrasplenic, subcapsular, or perisplenic area.