الفهرس 
Surgical anatomy and embryology of portal veinOnly 14 pages are availabe for public view
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Abstract
• Normal portal pressure is generally defined between 5 and 10mm Hg. Once the portal pressure rises to 12mm Hg or greater called portal hypertension and many, complications can arise, such as and ascites. Indeed, esophageal varices are responsible for the main complication of portal hypertension , massive upper gastrointestinal hemorrhage and other complication caused by portal hypertension which we will discussed in this work.( Lubel JS et al .2005 )
• Esophageal varices are the major complication of portal hypertension. It is detected in about 50% of cirrhosis patients, and approximately 5–15% of cirrhosis patients show newly formed varices or worsening of varices each year. ( Zhang C et al 2010 )
• Management of esophageal varies including Primary Prophylaxis of the varices and prevention the esophageal hemorrhage to be happened by nonselective beta-blocker, Band ligation of moderate esophageal varices or placement of TIPS, or surgical shunting should be considered in active variceal bleeding . ((Tripathi D et al , 2009 ).
• Also portal hypertension causes pathological changes to gastric mucosa as is characterized by more or less typical gastric mucosal lesions presenting in patients with portal hypertension (either pre-hepatic or hepatic). ( Primignani M et al . 2000).
• endoscopy still remains the chief diagnostic method to diagnose portal hypertension gastropahty. (Stewart CA et al , 2003)
• Gastric antral vascular ectasia (GAVE) also presented in portal hypertension pathological changes in stomach which is characterized by the presence of red spots without a background mosaic pattern that are typically located in the gastric antrum. ( Ward EM et al, 2004)
• Morphology changes in small intestine ( portal hypertension jejunopathy ) as defined by the presence of ectatic capillaries and venules in the villi, with an increase in the number of vessels.( CarithersRL Jr et al,2000)
• Histology shows that there is multiple changes in intestinal villi vessels in general dilated, ectatic vessels as the characteristic feature, with variable degrees of oedema and thickening of the muscularis mucosae but no significant increase in the amount of infiltrate. (Ghoshal UC ,et al 2001)
• Also pathological changes to large bowel happened with portal hypertension called Colorectal portal hypertensive colopathy . ((Ito K , et al ,2005 )
• PHC was considered to be present if there were nonspecific inflammatory changes, resembling the lesions found in subjects with inflammatory chronic colitis and defined as granularity, diffuse hyperemia, edema and friability in mild grades , and lesions such as vascular ectasias, angiodysplasia, arterial spider, and diffuse cherry red spots, in severe grades. (Bini EJ et al , 2000 ) .
• portal hypertension may also presented by rectal varices and were defined as large venous structures at or just proximal to anus and were subdivided into internal and external hemorrhoids. ( Chung RT et al,2001).
• The diagnosis of rectal varices could be missed and can sometimes be fatal , The cited frequency of rectal varices in cirrhosis varies from 44% to 89%. ( Ory G, et al 2001).
• Rectal vaices can be diagnosed by Endoscopic rectal ultrasound , transvaginal ultrasound , sigmoidoscopy and pelvic CT . ((Ghoshal UC et al,2000).
• portal circulation , in particular the contribution of the inferior mesenteric vein , can be evaluated in a relatively non invasive way by per rectal portal scintigraphy (Zuberi BF et al ,2000).
• In patients with portal hypertension there is other complication which is portal hypertensive biliopathy’’ (PHB) refers to abnormalities of the entire biliary tract including intrahepatic and extrahepatic bile ducts, cystic duct and gallbladder ( Bayraktar Y et al,2000).
• This is most probably related to longstanding portal hypertension that results in the development of large collaterals in the biliary region with the formation of a typical portal cavernoma . (Dhiman RK et al ,1999).
• Clinical presentation of HRS maybe Asymptomatic or Chronic cholestasis, likely to be caused by biliary stricture. Biliary pain or acute cholangitis, (Chandra R et al 2001). ]
• Hepatorenal syndrome (HRS) is a unique, functional form of potentially reversiblerenal failure that occurs in the presence of severe acute or chronic liver disease. (Garcia-Tsao G, et al,2008).
• Patients with protracted ascites frequently develop spontaneous bacterial peritonitis and subsequent HRS.( Kuiper JJ et al , 2007)
• Management of HRS should be in an intensive care setting with an initial search for precipitating events followed by treatment or correction of identified risk factors. (Fernandez J, et al ,2006)
• Diuretics should be limited, and potential nephrotoxic drugs such as nonsteroidal anti-inflammatory drugs discontinued. (Gluud LL, et al,2006)
• In patients with massive ascites and possible compartment syndrome of the abdomen, large-volume paracentesis accompanied by intravenous (IV) albumin (8 g/L of ascites fluid removed) may help.( Ortega R et al,2002).
• Hemodialysis is not indicated in the treatment of patients with HRS . (.( Wong F, et al , 2004)
• Liver transplantation is the definitive therapy for HRS(Weismuller TJ, et al ,2008) .
• Hypersplenism is a common complication of massive congestive splenomegaly in patients with cirrhosis and Portal hypertension. (.( Peck-Radosavljevic M et al ,2001)
• Ascites is defined as pathologically accumulated fluid in the peritoneal cavity. Uncomplicated ascites can be divided into three grades (Table 2) . (Moore KP, et al,2003).
• Spontaneous bacterial peritonitis (SBP) is a bacterial infection of ascites without definite evidence of a surgically treatable, intra-abdominal origin of infection.( Mitzner SR, et al , 2000).
• Clinical suspicion is important in the diagnosis of SBP, as the typical symptoms and signs of SBP, which include fever, abdominal pain, and leukocytosis, may be masked in patients with cirrhosis.[ (Castellote J et al , 2003)
• Prevention of Spontaneous bacterial peritonitis , Subgroups of cirrhotic patients who are at increased risk of SBP (include those with (i) prior episodes of SBP, (ii) active upper gastrointestinal bleeding, and (iii) low ascitic protein level (< 1.0 g/dL). Patients with prior episodes of SBP clearly benefit from oral norfloxacin (400 mg/d), which reduces SBP recurrence and lowers the cost of treatment.( Wong F et al , 2005)
• We conclude that portal hypertension as a complication from liver cirrohosis causes many pathological changes to gastro-intestinal track which are fatal to the patient .