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With a general lack of level I evidence to guide clinical decisions erectile dysfunction pills natural purchase on line viagra super active, there continues to be controversy surrounding some of these putative risk-lowering methods. We begin this chapter with a brief review of the normal host defenses preventing the entry of infectious organisms into the liver, biliary system, and pancreas. These same organisms may also pass through the liver to access the systemic circulation, potentially leading to sepsis and septic shock. These pathologic states do not normally occur in the healthy human because of defense mechanisms that exist at multiple organ-system levels. In this section, we are interested in those mechanisms specific to the hepatobiliary system and pancreas. In addition to absorbed nutrients, portal venous blood also contains enteric bacteria and toxins that may result in illness if not appropriately cleared by the liver. The second pathway into the liver is via retrograde entry through the biliary system. Organisms already present within the systemic circulation may also enter the liver via a third pathway-the arterial inflow. Both the liver and the biliary system contain important defense mechanisms that prevent enteric organisms from establishing infection within the liver. Generally, defense mechanisms are categorized into three types: physical, chemical, and immunologic (Table 12. The single most important mechanism within the liver is the immunologic defense provided by Kupffer cells. They are derived from circulating monocytes and represent almost 90% of the tissue macrophages present in the human body. Kupffer cells are constantly exposed to enteric organisms and endotoxins, leading to their activation as phagocytes. Once activated, Kupffer cells also release various cytokines, prostanoids, nitric oxide, and reactive oxygen species that contribute to their immune function (see Chapters 7, 10, and 11). Additionally, Kupffer cells indirectly regulate the phenotype of surrounding hepatocytes, stellate cells, endothelial cells, and other immune cells present in the liver (Bilzer et al, 2006). Without Kupffer cells, enteric organisms and their toxins entering the liver through portal venous blood flow would freely pass into the systemic circulation. Portal hypertension, whether from presinusoidal, sinusoidal, or postsinusoidal causes, undermines the ability of the Kupffer cells to clear portal venous inflow of enteric organisms and toxins. Portal venous obstruction results in the shunting of portal venous blood to the systemic venous circulation through the development of collateral pathways. Tight junctions prevent mixing of blood and bile within the liver by forming a physical barrier between the bile canaliculi and hepatic sinusoids. Biliary ductule epithelial cells each contain a single cilium that helps move bile toward the extrahepatic ducts (Gilroy et al, 1995; Itoshima et al, 1977). Mucus produced by the extrahepatic bile ducts prevents prolonged contact between the ductal epithelium and bacteria. Both of these features promote forward flow of bile out of the liver, thus preventing retrograde ascent of any bacteria that have entered the biliary system. Bile salts are a chemical barrier to infection and have several important properties (see Chapter 8). First, they have both bacteriostatic and bactericidal properties (Stewart et al, 1986; Sung et al, 1993) capable of maintaining the normal balance of intestinal flora. Second, they have a trophic effect on the intestinal epithelium, allowing it to maintain its own effective barrier against bacterial translocation (Stewart et al, 1986). The biliary system also contains immunologically active substances that combat infection, including immunoglobulin A (Emmrich et al, 1998; Scott-Conner & Grogan, 1994), fibronectin (Wilton et al, 1987), and complement factors (Sumiyoshi et al, 1997). An important difference is that there are no Kupffer cell analogues in the pancreas. The reason for this lies in the fact that the pancreas does not represent a "window" to the systemic circulation. Thus, unlike the liver, it does not represent a defense against enteric microorganisms attempting to enter the systemic circulation. The biliary system has a number of ways to prevent retrograde invasion into the liver by pathogenic microorganisms. From a physical barrier standpoint, the sphincter of Oddi is effective at preventing bacterial ascent into the liver. Microscopic physical defense mechanisms Remote-Site Infections Remote-site infections include those infections distant from the incision and operative field: respiratory tract infections, urinary tract infections, and catheter-related bloodstream infections. Patient-Related Risk A recent review discusses the important risk factors generated by the patient (Kirby et al, 2009). Some of these risk factors may not be modifiable at the time of operation, but it is important to be aware of them while the patient receives care. It may be an important clinical adjunct for both surgeon and patient alike in the preoperative decisionmaking process. It cannot be overemphasized that the mitigation of infectious risk occurs at all phases of patient care (Tables 12. Many of these general preventive measures were incorporated into a perioperative surgical care bundle and applied to patients undergoing pancreaticoduodenectomy in a retrospective study conducted at Thomas Jefferson University. The results showed a lower rate of wound infections in patients subjected to the surgical care bundle (7. It must also be kept in mind that any patient can experience an infectious complication from the introduction of outside microbes into the wound through a break in sterile technique.

In the right midclavicular line erectile dysfunction frequency purchase viagra super active 100 mg on-line, the normal mean length is 10 cm, with a standard deviation of 1. In most patients the measurement of liver length suffices, but hepatic shape can be variable, and thus threedimensional ultrasound volumetric analysis can aid evaluation (Treece et al, 2001; Wilson et al, 2009). The vascular landmarks that define the Couinaud segmental anatomy are well seen by ultrasound (Lafortune et al, 1991; Soyer et al, 1994). Images are best obtained in the subcostal or intercostal approach, with the patient in a supine or left lateral decubitus position. The proximal portion of the left portal vein is extrahepatic and courses anteriorly and leftward, and thus it is often best visualized in the subxiphoid region, whereas the right portal vein and its bifurcation are best visualized with a subcostal approach. Hepatic Masses Liver Mass Detection and Characterization Echogenicity is the dominant factor determining lesion conspicuity on ultrasound. Markedly hypoechoic or hyperechoic lesions may be readily detected and characterized by ultrasound, even when small (Eberhardt et al, 2003). Larger masses that have echogenicity similar to adjacent liver may be more difficult to appreciate. Lesion size and body habitus are significant factors that influence lesion detection (Eberhardt et al, 2003). On gray scale ultrasound, liver masses are differentiated by internal architecture and are described as cystic, hypoechoic, or hyperechoic relative to the liver. Electromagnetic sensors placed near the scanning area and sensors attached to the ultrasound probe allow tracking of transducer position and orientation. Similar instrumentation allows global positioning system navigation for needle tracking and volume acquisition. Ultrasound contrast agents are intravenously injected microbubbles that are highly echogenic and oscillate in an ultrasound field to enhance ultrasound signal in gray scale, color, and spectral Doppler. Bubbles are capable of transpulmonary passage for left-side blood pool enhancement. Ultrasound contrast agents are purely intravascular and do not diffuse into the interstitium. Ultrasound is sensitive to extremely low concentrations of contrast due to amplification of echoes from resonating microbubbles in the blood pool. To obtain images of best quality, ultrasound scanning techniques should optimize imaging settings, which can vary depending on the contrast agent. Microbubbles stay in the circulation, allowing continuous assessment as the contrast agent traverses the imaging field. Observations are made of the liver and focal liver lesions, including wash-in, peak enhancement, and washout. Lesions enhance differently than background parenchyma and thus will show increased conspicuity within the enhanced parenchyma. Sustained enhancement, meaning that the lesion remains isoechoic or hyperechoic to the liver, is a favorable sign and associated with benignity. These patterns of enhancement can be used to differentiate benign from malignant focal hepatic lesions and will be described in the lesion subsections (Brannigan et al, 2004; Ding et al, 2005; Wilson & Burns, 2006). Contrast agents also improve diagnostic accuracy and diagnostic confidence (Albrecht et al, 2003; Albrecht et al, 2004; Blomley et al, 1999; Bryant et al, 2004; Harvey et al, 2000; Quaia et al, 2004; Strobel et al, 2009). Ultrasound contrast agents are not nephrotoxic, and impaired renal function is not a contraindication (Jang & Yu, 2009). Ultrasound contrast research is a rapidly evolving and expanding field, with many potential applications, including imaging, potentiation therapy, and drug delivery. A confident diagnosis of simple hepatic cyst can be made on ultrasound, and no further evaluation is required. Blood vessels and arteriovenous fistulas or aneurysms may appear cystic on gray scale ultrasound, yet can easily be differentiated from simple cysts by demonstrating internal blood flow on Doppler imaging. Lymphomatous masses are markedly hypoechoic and may mimic simple cysts on gray scale ultrasound, yet will demonstrate internal vascularity on color Doppler. When cysts are innumerable and also present in the kidneys or pancreas, polycystic disease should be considered. Cystic masses are deemed complex when there are internal echoes within the cyst fluid, irregular or thickened walls, mural nodularity, solid areas, or calcification. Differential diagnosis of complex cystic masses includes hemorrhage, infection, and neoplasm. Cysts with internal hemorrhage may have internal solid components, septations, and layering debris, but with no detectable vascularity. Hepatic hematomas from trauma initially appear hyperechoic and over time will evolve to become hypoechoic and cystic (Korner et al, 2008; McGahan et al, 2006). Echinococcal cysts have a variable appearance and may appear as simple fluid-filled cysts, may contain wavy membranes from a rupture and detached endocyst, may contain daughter cysts and/or echogenic material, or they may show calcification (Lewall & McCorkell, 1985). When hydatid cysts are infected, they lose their characteristic sonographic appearance and become diffusely hyperechoic (see Chapter 74). Cystic neoplasms, such as biliary cystadenoma and cystadenocarcinoma, may be multilocular, with cystic locules demonstrating different echogenicities depending on the cystic fluid content (see Chapter 90B). They may have mural nodularity, nodular thickened septations, and mural or septal calcifications (Buetow et al, 1995; Levy et al, 2002). Theabscess(asterisk) contains complex fluid and has posterior acoustic enhancement (arrows). Larger hemangiomas often lack characteristic features because of central fibrosis, necrosis, and myxomatous degeneration.

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An association with infection by Clonorchis sinensis and Ascaris lumbricoides has been implicated in the past (Fung erectile dysfunction vitamin e order genuine viagra super active, 1961) and is still often regarded as causally significant (Rana et al, 2007) (see Chapter 45). It is indisputable that clonorchiasis is a serious infection that may cause structural changes in the intrahepatic and extrahepatic bile ducts (Hou, 1956). Even if clonorchiasis and ascariasis are merely coincidental infections, they may become a nidus for stone formation (Teoh, 1963). Endoscopic retrograde cholangiopancreatography showing early recurrent pyogenic cholangitis changes with extensive branching and dilatation of the left intrahepatic ducts proximal to the intrahepaticductalstrictures. The results of repeated infection are progressive biliary epithelial and hepatocellular damage, as discussed previously. Itisweblike,andproximaldilatationisseen, with stones above and below the stricture. Strictures in the hepatic ducts also extend over a short distance and are usually intrahepatic, but they may extend C. Left duct involvement alone is found in 40% of cases of intrahepatic disease, right duct involvement alone in 20%, and involvement of both ducts in 40%. No satisfactory explanation has been offered for this finding, but it has been suggested that the left duct is more horizontal, and bile in the left duct may not drain as well as bile in the right duct. Dilated segments taper toward the strictures, which are thick and fibrous; when operative plastic repair of such strictures is attempted, restenosis is common as a result of ongoing fibrotic changes in the diseased ductal tissues, and failure can be expected in most cases. When stones are found in the gallbladder, disease is invariably present elsewhere. In the acute attack, and when common duct obstruction is severe, the gallbladder may be grossly distended, and empyema, gangrene, or perforation may develop. When a normal gallbladder is left behind after drainage procedures to the common duct, the risk of a complication from the gallbladder that would require surgery is small. In the fresh state, the stone surface is covered with mucus or a film of viscous bile. In some stones, the outer color may be almost black from prolonged exposure to bile; in others, it is orange or green. B, Computed tomographic scan of the same patient shows the typical featuresofthiscondition. Some stones show no organized structure and disintegrate with slight compression into irregular, powdery clumps. A nidus may sometimes be identified, and microscopic examination of this area may show dead parasites or clumps of bacteria or cells (Teoh, 1963). In approximately 10% of patients, stones are absent, and the bile duct is filled with biliary debris, termed biliary mud. This debris is composed of mucus, pus, parasites, altered bile products, microcalculi, and desquamated epithelium, all mixed to form a thick, porridge-like material that exudes from the duct when it is opened. In an acute attack, this soft, infected material with or without stones is more frequently encountered. At operation for an acute problem, the liver appears "cholangitic": congested, bile stained, soft, and prone to bleeding easily. In the quiescent phase, avascular adhesions are found between the surface of the liver and the parietal peritoneum- evidence of previous, resolved acute episodes. In long-standing cases, the adhesions are dense and vascular and contain pockets of pus, which are caused by rupture of cholangitic liver abscesses into the peritoneal cavity. When the left lobe is atrophic, compensatory hypertrophy of the right lobe is seen. Even when the external appearance is normal, intrahepatic disease may be extensive, and stones are easily palpable through the surface. Biliary cirrhosis and liver failure are possible complications (Jeng et al, 1989) and usually follow long-standing severe disease that has failed to improve with multiple operations, some of which may be associated with stricture of the biliaryenteric anastomosis (see Chapters 31 and 42). When cirrhosis has developed, portal hypertension and bleeding esophageal varices may ensue (see Chapter 76). Further corrective biliary surgery is feasible only after decompression by portosystemic shunting (see Chapters 85 to 87). Choledochoduodenal fistula is not serious, but it may be confusing to the endoscopist and the radiologist. Although rare, abscesses in the left liver may rupture into the pericardial cavity and cause cardiac tamponade (Fan & Wong 1997). Abscesses in the right liver may rupture to form a pleurobiliary or bronchobiliary fistula (Wei et al, 1982). A chronic abscess may be indistinguishable clinically, at surgery or on contrast studies, from cholangiocarcinoma, and it may be identified as such only through detailed histologic examination after resection. As with hepatolithiasis, an increased incidence of cholangiocarcinoma resulting from clonorchiasis has been noted (Hou, 1956; Ohta et al, 1984) (see Chapters 50 and 51). The almost constant presence of severe clonorchiasis in patients with cholangiocarcinoma supports a cause-and-effect relationship (Belamaric, 1973) (see Chapter 73). Cholangiocarcinoma is found in 2% to 13% of patients with intrahepatic stones (Chen et al, 1989; Chu et al, 1997; Ohta et al, 1984, 1988) (see Chapter 39). Autopsy studies suggest that recurrent cholangitis can induce progressive changes, leading to atypical epithelial hyperplasia and cholangiocarcinoma (Ohta et al, 1984). Recent studies of hepatolithiasis have identified two distinct neoplastic intraepithelial lesions preceding cholangiocarcinoma: (1) biliary intraepithelial neoplasm and (2) intraductal papillary neoplasm of the bile duct.