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C I R R H O S I S A N D P O R T A L

H Y P E R T E N S I O N
FRED S. BONGARD

he causes of portal hypertension vary with geographic location. Worldwide, the most common cause is infection with schistosomiasis, which causes presinusoidal brosis of the liver. In the United States, alcohol intake with resultant cirrhosis is the most common etiology. In Asia, where infection with hepatitis B is endemic, postin45 mg/L. A rapid infusion of saline was begun to correct hypotension, and blood was sent for type and cross-match. Emergent esophagogastroscopy found several large bleeding varices in the distal esophagus. An intravenous infusion of Pitressin was begun. Aspirate from the nasogastric tube cleared over the next 18 hours. Further evaluation found the patient to have moderate ascites, no encephalopathy, a serum albumin concentration of 2.8 mg/L, and a bilirubin concentration of 3.2 mg/L. He was assigned a Child B classication. Evaluation for possible portasystemic shunting found that the splenic and portal veins were both patent. After several days of resuscitation and stabilization, he underwent a selective portasystemic shunt. Two years after the procedure he stopped drinking and experienced no further episodes of bleeding, but had a decreased attention span and was often confused.

fectious cirrhosis is prevalent. Common to all causes of portal hypertension is an obstruction to blood ow within the portal venous system. The effects of portal hypertension range from subclinical to massive hematemesis. This chapter discusses the pathophysiologic mechanisms of portal hypertension, the dependence on etiology of clinical presentation, a scoring system for the severity of the disease, and approaches to both surgical and nonsurgical management.

CASE 1 ALCOHOLIC CIRRHOSIS AND PORTAL HYPERTENSION A 54-year-old chronic alcoholic consumed at least 2 pints of whiskey a day for the past 13 years. On arising the morning of presentation, he began to feel nauseated and started to vomit dark red blood with clots shortly thereafter. On arrival at the hospital, he had a BP of 100/60 mmHg and an HR of 120 bpm. After several more bouts of bloody emesis, a nasogastric tube was inserted, which produced several hundred milliliters of dark blood. Lavage was begun with 2 L of uid until the aspirate returned clear. Signicant laboratory results were as follows: Hb, 9.2 g/dl: PT, 16.4 seconds (control = 12.0 seconds); K+, 3.1 mEq/l; and BUN,

CASE 2 HEPATITIS AND PORTAL HYPERTENSION A 36-year-old Chinese immigrant developed hepatitis B at age 13. Since that time, she has had chronic active disease with a brotic liver and signs of portal hypertension. Two 155

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previous hospitalizations have been required for hematemesis, which responded to nonoperative therapy. Her latest episode of bleeding was worse than those in the past. Her Hb had fallen to 7.2 g/dl from her usual value of 12.5 g/dl. Emergent esophagoscopy demonstrated multiple large bleeding varices. Signicant laboratory values were as follows: albumin, 2.3 g/L; bilirubin, 4.1 g/L; PT, 15.3 seconds (control = 12.0 seconds). She was found to have moderate ascites, temporal wasting, and no encephalopathy. An NG tube was inserted and returned 750 ml of bloody uid. A continuous infusion of vasopressin was begun, but the bloody aspirate persisted and her Hb continued to fall. Repeat esophagogastroscopy was done and the bleeding varices injected with a sclerosant solution. Despite three sessions of sclerotherapy over the next 36 hours, she continued to bleed and developed a profound coagulopathy. On the fourth hospital day, her urine output fell, despite adequate uid resuscitation. In spite of dialysis and pressor support, she expired on the ninth hospital day.

GENERAL CONSIDERATIONS

he liver receives blood ow from the hepatic artery and from the portal vein. The hepatic artery arises from the celiac axis and terminates in the liver after branching into left and right tributaries. The portal vein begins at the conuence of the splenic and superior mesenteric veins behind the pancreas. It subsequently receives the inferior mesenteric vein before turning upward to enter the liver. Because of its position, it is susceptible to inammatory processes in the pancreas that may cause portal vein thrombosis. Two-thirds of hepatic blood ow is from the portal vein, although most of the oxygen supply to the liver is through the hepatic artery. Hepatic arterial ow changes reciprocally with alterations in portal venous ow. However, acute changes in hepatic arterial ow do not produce signicant increases in portal venous ow. Portal hypertension occurs when there is an obstruction to blood ow through the portal venous (mesenteric) system. The location of the obstruction is related to the etiology of the disease. Mesenteric ow to the liver proceeds through the portal vein to the liver, through the portal sinusoids, into the hepatic veins, and nally into the inferior vena cava. Portal hypertension is divided into three broad categories, prehepatic, hepatic, and posthepatic. Rarely, it may be produced by increased portal blood ow, which occurs with splenomegaly, an arterioportal venous stula, or with Bantis syndrome (primary splenic disease). Prehepatic causes are due to portal vein obstruction, which may follow congenital stenosis of the portal vein, thrombosis (following pancreatitis), or stenosis from extrinsic compression (e.g., tumor). Schistosoma cruzii is a parasite, particularly common in the Middle East, that causes presinusoidal brosis. This

prevents portal blood from owing normally through the hepatic system. Even though portal hypertension is created, it occurs before blood reaches the sinusoids and liver function remains normal. Alcoholic cirrhosis and hepatitis, as well as a number of chemical agents, cause postsinusoidal brosis, which initially prevents blood from leaving the liver, but eventually causes such signicant distortion that portal venous inow is affected and portal hypertension results. Unlike the situation with presinusoidal disease, alcoholic cirrhosis causes profound hepatic dysfunction, which ultimately results in liver failure. An uncommon variant of postsinusoidal disease occurs in the Budd-Chiari syndrome, in which hepatic venous or vena caval outow from the liver is limited, often by congenital stenosis, bands, or webs. This effectively constitutes a postsinusoidal obstruction and results in hepatic pathophysiology similar to alcoholic cirrhosis or viral hepatitis. When portal venous pressure is increased, alternate pathways for mesenteric blood ow develop. Such collateral pathways are anatomic connections between the portal and systemic circuits, which normally have little or no ow through them. However, as portal pressure increases, these pathways enlarge and shunt blood away from the portal system to the lower resistance systemic veins (Fig. 22.1). The portasystemic collaterals of greatest importance are in the esophagus, the pelvic circulation, the retroperitoneum, and the abdominal wall. The coronary (left gastric) vein connects the portal and systemic circuit through the veins of the esophagus and the azygos vein, which empties into the superior vena cava. When portal pressure increases, blood ows in a retrograde fashion (hepatofugal) through the esophagus to the low pressure systemic venous circuit. Veins that are usually very small, such as the esophageal submucosal veins, become engorged to carry the increased ow from the mesenteric circulation. The enlarged submucosal varices may erode through the mucosa and bleed into the lumen, resulting in severe hematemesis. Because of the increased pressure and ow within the collaterals, the hemorrhage tends not to stop once it has begun. Another important collateral pathway exists in the rectum between the superior hemorrhoidal veins of the portal system and the middle and inferior hemorrhoidal veins of the systemic circuit. Increased ow within these collaterals produces large hemorrhoidal veins that are easily damaged and may bleed profusely. In the retroperitoneum, in the veins of Retzius, which connect the mesenteric and peritoneal veins, hypertrophy occurs as ow increases. The abdominal wall contains communication between the superior and inferior epigastric veins and supercial systemic veins. The dilated veins produce a characteristic vascular pattern of radiating vessels around the umbilicus referred to as caput medusae. In addition to the formation of varices and hemorrhoids, portal hypertension has other deterimental physiologic effects. Because mesenteric blood is shunted away from the liver, normal hepatocellular function cannot occur.

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FIGURE 22.1 Several pathways (portasystemic collaterals) develop so that blood can pass around the high pressure portal system into the systemic circuit. The major connections are between the (1) esophageal and azygos veins, (2) gastric veins and inferior vena cava, (3) retroperitoneal veins, (4) veins of the abdominal wall (caput medusae), and (5) hemorrhoidal veins.

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Hepatic encephalopathy is a reversible syndrome that occurs when toxins absorbed from the gut adversely affect the brain and central nervous system. The toxins arise from the action of bacteria on absorbed protein within the gut. Encephalopathy is particularly severe with increased protein intake, after episodes of esophageal variceal hemorrhage, infections, azotemia, and hypokalemic metabolic alkalosis. False neurotransmitters, formed in the gut, are thought to cross the blood-brain barrier and result in encephalopathy. The aromatic amino acids (tryptophan, tyrosine, and threonine) have increased access to the central nervous system where they serve as precursors of false transmitters. Additionally, -aminobutyric acid, which is formed by colonic bacteria, passes across the blood-brain barrier and serves as an inhibitory neurotransmitter. Ammonia is also formed by colonic bacteria and is normally converted to glutamine by the liver. When hepatofugal ow is present, increased ammonia concentrations are found in both arterial blood and cerebrospinal uid. When perisinusoidal pressure increases sufciently, uid transudation occurs. If production exceeds the reabsorptive capacity of hepatic lymphatics, ascites are produced. Protein rich ascites results in loss of volume from the intravascular space into the peritoneum. The physiologic response to this intravascular volume contraction includes salt and water retention due to the actions of aldosterone. The patient becomes hypokalemic, hypernatremic, and oliguric (Case 1). Ascites produces abdominal distention and may eventually result in spontaneous bacterial peritonitis if infection occurs.

Portasystemic collaterals of greatest importance are in the esophagus, pelvic circulation, retroperitoneum, and abdominal wall Because mesenteric blood is shunted away from the liver, normal hepatocellular function cannot occur Hepatic encephalopathy is a reversible syndrome that occurs when toxins absorbed from the gut adversely affect the brain and central nervous system

DIAGNOSIS

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In United States, alcohol intake with resultant cirrhosis is most common etiology Common to all causes of portal hypertension is an obstruction to blood ow within the portal venous system Two-thirds of hepatic blood ow is from the portal vein, although most of the oxygen supply to the liver is through the hepatic artery Three broad categories of portal hypertension: prehepatic, hepatic, and posthepatic Alcoholic cirrhosis and hepatitis, as well as a number of chemical agents, cause postsinusoidal brosis, which initially prevents blood from leaving the liver, but eventually causes such signicant distortion that portal venous inow is affected and portal hypertension results Unlike the situation with presinusoidal disease, alcoholic cirrhosis causes profound hepatic dysfunction, which ultimately results in liver failure Collateral pathways are anatomic connections between the portal and systemic circuits, which normally have little or no ow through them; however, as portal pressure increases, these pathways enlarge and shunt blood away from the portal system to the lower resistance systemic vascular resistance

ortal hypertension and variceal bleeding are sequelae of the underlying hepatic disease. Patients with cirrhosis will typically exhibit malnutrition, palmar erythema, encephalopathy, ascites, and jaundice. Splenomegaly is the most common physical nding, and is present in 80% of those with portal hypertension, regardless of the cause. Bleeding occurs in approximately 40% of those with cirrhosis. The rst step in the treatment of presumed variceal hemorrhage is vigorous resuscitation. Fluid administration should consist of both balanced salt solution and red blood cells as required. Because the synthetic capacity of the liver may be severely impaired, prothrombin time (PT) should be checked and fresh frozen plasma administered as required to correct any coagulopathy. A nasogastric tube should be inserted for gavage and aspiration of clots, as well as to monitor continuing hemorrhage. A Foley catheter should be placed so that urine output can be used to guide further uid resuscitation. If shock is present, or if the patient does not respond to initial resuscitative measures, central hemodynamic monitoring should be instituted. Upper gastrointestinal endoscopy is the most useful procedure for the diagnosis of variceal hemorrhage. It should be performed as soon as possible after the patient is hemodynamically stable. Varices appear as large, bluish, submucosal vessels that run longitudinally along the length of the esophagus. Bleeding varices are easily identied, although fresh adherent clot may be present, indicating that hemorrhage was present recently. Occasionally gastric varices may be identied; this is particularly true when splenic vein thrombosis is the cause of portal hypertension. Radiographic studies such as an upper gastrointestinal series are not helpful in identifying the source of hemorrhage, although they may conrm the presence of varices. Laboratory studies including electrolytes, clotting parameters (PT and PTT [partial thromboplastin time]), blood type, platelet count, serum albumin, bilirubin, and liver and renal function tests should be obtained. The Child classication is a simple index of functional liver disease (Table 22.1) and should be calculated for all patients with portal hypertension. The Child-Pugh classication (Table 22.1) is the most recent modication. Earlier ver-

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sions used nutritional status (good, fair, poor) instead of elevations in the PT. Mortality rate, both with and without surgery, is directly related to the Child classication.

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Even when known portal hypertension and varices present, one-half of those presenting with acute hemorrhage will be bleeding from a source other than varices

Splenomegaly most common physical nding; present in 80% of those with portal hypertension, regardless of cause Bleeding occurs in approximately 40% of those with cirrhosis Upper gastrointestinal endoscopy the most useful procedure for diagnosis of variceal hemorrhage; it should be performed as soon as possible after patient is hemodynamically stable Radiographic studies such as an upper gastrointestinal series are not helpful in identifying the source of hemorrhage, although may conrm presence of varices Mortality rate, with and without surgery, is directly related to Child classication

TREATMENT

DIFFERENTIAL DIAGNOSIS

pper gastrointestinal hemorrhage may be caused by a number of etiologies (see Ch. 20). Even when known portal hypertension and varices are present, one-half of those presenting with acute hemorrhage will be bleeding from a source other than their varices. Sources include gastritis and peptic ulcer disease. Therefore, it is imperative that the diagnosis of bleeding varices be conrmed by gastroesophagoscopy before any therapy is begun. Other causes of hematemesis that are common among alcoholics and those with cirrhosis include: epistaxis, Mallory-Weiss syndrome, gastritis, and peptic ulcer disease.

TABLE 22.1 Child-Pugh classication of functional status in liver disease


CLASS: A RISK: LOW Ascites Encephalopathy Serum albumin (g/dl) Serum bilirubin (mg/dl) Prothrombin time (seconds above control) Absent None >3.5 <2.0 <4.0 B MODERATE Slight to moderate Grades III 3.03.5 2.03.0 4.06.0 C HIGH Tense Grades IIIIV <3.0 >3.0 >6.0

(From Way L: Current Surgical Diagnosis and Treatment, 10th Ed. Appleton & Lange, E. Norwalk, CT, 1994, with permission.)

he goal of the acute management of variceal bleeding is to stop the hemorrhage as quickly as possible since the death rate increases quickly when more than 10 units of blood have been transfused. The mortality rate among those with acute variceal hemorrhage is 35%. After uid resuscitation and esophagogastroscopy have been completed, control of the hemorrhage should begin. Vasopressin and terlipressin (triglycyl lysine vasopressin) are compounds that lower portal blood ow and portal pressure by constricting splanchnic arterioles. When given intravenously (vasopressin 0.4 units/min), they control bleeding in 80% of patients. Because they are vasoconstrictors, they may produce myocardial and visceral ischemia. Concomitant administration of isoproterenol or nitroglycerin helps to ameliorate these side effects. Octreotide acetate (somatostatin) has similar effects on the splanchnic circulation as vasopressin, but without many of the side effects. It is given as an initial bolus of 100 g followed by a continuous infusion of 25 g/hr for 24 hours. When vasopressin does not control the hemorrhage, mechanical tamponade with a balloon catheter is indicated. Several styles of balloons are available, but they all work on a similar principle. Most have two balloons, one gastric and one esophageal. After the tube has been inserted, the gastric balloon is inated and pulled into position at the esophagogastric junction (the position must be conrmed radiographically). The balloon occludes the venous inow from the stomach into the bleeding varices. If hemorrhage does not stop, the esophageal balloon should be inated. A manometer must be used to ensure that the balloons are not overinated, which might cause gastric or esophageal rupture. Balloon compression alone is successful 70% of the time. When used in combination with vasopressin, hemorrhage is controlled in 95% of patients. The balloons are deated within 24 hours after bleeding stops. The esophageal balloon should always be deated before the gastric balloon. In addition to the possibility of esophageal perforation, the other signicant side effect is aspiration of saliva with subsequent pneumonia. When small bleeding sites can be identied with the esophagogastroscope, injection of a sclerosing agent into the variceal lumen causes sclerosis and thrombosis of the vessel. Endoscopy should be repeated within 48 hours and for several weeks thereafter to treat residual varices. Sclerotherapy controls 8095% of patients, although about one-half will rebleed during the same hospitalization.

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A minimally invasive radiologic procedure is now available for emergency portasystemic decompression. The transjugular intrahepatic portasystemic shunt (TIPS) procedure involves uoroscopic placement of a catheter in the liver substance (via the vena cava and hepatic veins), which is used to create a shunt between the two circulations. The shunt usually stays open for 1 year and is particularly useful in those being considered for liver transplantation. Emergent surgery for acute variceal hemorrhage is required infrequently because of the success of sclerotherapy and vasopressin. Operative procedures fall into two groups: ligation and shunt. The Sugiura procedure consists of splenectomy, proximal gastric devascularization, vagotomy, pyloroplasty, esophageal devascularization, and esophageal transection and reanastomosis. Simple esophageal transection and reanastomosis with a mechanical stapler is used for variceal ligation in some centers. Splenectomy is a nonshunting procedure performed when portal hypertension is due to splenic vein thrombosis, which may occur following pancreatitis or other inammatory processes. Splenectomy, for this indication, lowers portal pressure, reduces gastric varices, and effectively prevents further hemorrhage. Shunting procedures are usually performed on a semielective basis in good risk (Child A and B) patients whose acute bleeding has stopped. Operative shunt procedures are either selective or nonselectivethat is, they either selectively decompress the esophageal varices or decompress the entire portal/mesenteric bed. Nonselective operations are far more common and consist primarily of end-to-side or side-to-side shunts. These terms are used to describe how the portal vein (or one of its tributaries) is connected to the inferior vena cava to create the shunt. In an end-toside operation, the portal vein is transected before it enters the liver. The vein on the hepatic side is ligated. The end of the proximal portal vein is connected to the side of the inferior vena cava (Fig. 22.2A & B). Hence, all of the portal blood ow is shunted into the systemic circulation. Although this procedure acutely reduces portal pressure and may control ascites, it frequently worsens encephalopathy because all of the products of digestion bypass the liver and are routed into the systemic circulation. A side-to-side (nonselective) portacaval shunt anastomosis connects the side of the portal vein to the side of the inferior vena cava (Fig. 22.2A & B). This procedure is differentiated from the end-to-side operation in that the liver is allowed to decompress while potentially maintaining some prograde (hepatopedal) flow through the portal vein. Like the end-to-side shunt, the major postoperative complication of the side-to-side shunt is worsened hepatic encephalopathy. The major variant is the mesocaval shunt in which the side of the superior mesenteric vein is connected to the side of the inferior vena cava (Fig. 22.2C). The advantage of the mesocaval shunt is that it is technically easier (does not require dis-

section at the porta hepatis) and can use a synthetic graft to connect the vessels. Its disadvantage is that the graft may clot quickly due to relatively low flows. The distal splenorenal shunt is the only commonly performed selective shunt. In contradistinction to the end-to-side and end-to-end shunts, the distal (Warren) splenorenal shunt is selective because it compartmentalizes the portal ow, and shunts only that portion contributing to the bleeding varices (Fig. 22.3). By maintaining prograde ow through the liver, it is thought to have a lower incidence of encephalopathy than other operations. The increased portal ow may, however, produce ascites, and therefore should not be used in people with moderate or severe ascites before surgery. Liver transplantation should be considered in young patients who have survived an episode of variceal bleeding. Candidates should have abstained from alcohol, or should have any systemic disease under control. If a patient under consideration for liver transplantation rebleeds, a TIPS procedure or a mesocaval shunt are the procedures of choice since they do not require dissection at the hepatic hilum, which would make subsequent transplantation more difcult technically.

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When given intravenously (vasopressin 0.4 units/min controls bleeding in 80% of patients When vasopressin does not control the hemorrhage, mechanical tamponade with a balloon catheter is indicated Balloon compression alone is successful 70% of the time; when used in combination with vasopressin, hemorrhage controlled in 95% of patients When small bleeding sites can be identied with the esophagogastroscope, injection of a slcerosing agent into the variceal lumen causes sclerosis and thrombosis of the vessel Sclerotherapy controls 8095% of patients, although about one-half will rebleed during same hospitalization Emergent surgery for acute variceal hemorrhage required infrequently because of the success of sclerotherapy and vasopressin Operative shunt procedures are either selective or nonselective; that is, they either selectively decompress the esophageal varices or decompress the entire portal/mesenteric bed Liver transplantation should be considered in young patients who have survived an episode of variceal bleeding

FOLLOW-UP

onoperative therapy is now the standard treatment for patients acutely bleeding from varices. Hemorrhage can be controlled in 90%, although the early rebleeding rate is 30%. When medical and surgical treatment are compared, most trials have shown that surgical therapy is

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B FIGURE 22.2 (A) A side-to-side portasystemic shunt connects the side of the portal vein (shaded) to the side of the inferior vena cava. This allows the liver to decompress (retrograde) through the shunt while allowing prograde ow from the viscera into the inferior vena cava. (B) An end-to-side portasystemic shunt connects the proximal end of the portal vein (shaded) to the side of the inferior vena cava. Unlike a side-to-side shunt, the liver cannot decompress. (Figure continues.)

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C FIGURE 22.2 (Continued) (C) The mesocaval shunt is a type of side-to-side portasystemic shunt. Rather than connecting the portal vein and inferior vena cava directly, a short graft is interposed between them. Either autogenous vein or prosthetic can be used. This operation is technically easier than a side-to-side shunt (Fig. A) and does not disturb the anatomy in the right upper quadrant, making a subsequent liver transplant easier.

FIGURE 22.3 The distal splenorenal (Warren) shunt is created by disconnecting the distal splenic vein and turning it down to connect with the renal vein. This operation was thought to compartmentalize portal ow by returning blood from the high pressure esophageal veins into the renal vein and from there into the vena cava. This leaves undisturbed the portal ow from the superior and inferior mesenteric veins. In time, the shunt looses its selectivity. Increased ascites production is a common complication of the procedure.

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better at preventing subsequent bleeding than is medical treatment alone. Disturbingly, neither medical nor surgical therapy decrease the overall mortality rate from portal hypertension, which is directly related to the patients Child classication. Furthermore, except for patients with extremely poor liver function (Child C), those treated by chronic sclerotherapy have a lower mortality rate than those treated with a portasystemic shunt. There is no proven benet of prophylactic portasystemic shunting in patients with esophageal varices who have not experienced an episode of variceal bleeding. Encephalopathy, ascites, and the hepatorenal syndrome are common complications of cirrhosis, portal hypertension, and shunt procedures. Encephalopathy is aggravated by increased amounts of intestinal protein, regardless of origin. It is worsened by intestinal hemorrhage, constipation, and continued alcoholism. It may be particularly problematic after an end-to-side portacaval shunt. Patients usually have increased arterial ammonia levels along with characteristic changes on electroencephalography. Acute treatment consists of stopping all dietary protein intake and cleansing the bowel using purgatives, enemas, and antibiotics. Lactulose, a minimally absorbed disaccharide, acidies the colon and produces a catharsis thereby limiting protein absorption. Neomycin (24 g/day), a luminal antibiotic, may be helpful by reducing the endemic ora that convert protein to ammonia. Chronic encephalopathy is best treated by limitation of protein intake to less than 50 g/day and consumption of a high carbohydrate diet. Ascites is treated with chronic diuretic administration aimed at reducing the response to aldosterone. When a patients 24-hour urinary sodium is between 5 and 25 mEq, diuretic therapy is indicated. Spironolactone, an aldosterone inhibitor, is the drug of choice and is started at 25 mg three times a day, and advanced until ascites are controlled. The objective is to produce a weight loss of 0.50.75 kg/day until a stable weight is reached. Salt and water restriction is required only in the most difcult cases. Another diuretic, such as furosemide, may be used when a satisfactory diuresis is not achieved with spironolactone. When diuretics (400 mg/day) are not effective in controlling or reducing ascites, a peritoneovenous shunt (LeVeen) may be performed. This procedure consists of placing a tube with a mechanical one-way valve between the peritoneal cavity and the jugular vein. The low hydrostatic pressure within the jugular vein allows ascites to ow from the peritoneum into the superior vena cava. Newer tubes have small pumps that allow patients to transfer uid actively. Peritoneovenous shunts may also be used in those whose ascites are due to cancer. A functioning LeVeen shunt cannot completely eliminate ascites, but it makes the patient more responsive to diuretic therapy. The complications of shunt placement include peritonitis and disseminated intravascular coagulation (DIC). Post-

shunt DIC occurs in up to 50% of patients and is evidenced by increased brin split products and decreased platelet count. Bacterial peritonitis occurs commonly in patients with ascites and may produce a paucity of symptoms other than malaise and fever. It is diagnosed by aspirating a small amount of ascitic uid. Typical ndings include a white count greater than 250 cells/ml, and a protein concentration of less than 1 g/dl. The uid should be sent for microbiologic culture and sensitivity testing. Most cases have only one infecting organism such as Escherichia coli or pneumococcus. Treatment is with intravenous antibiotics. Polymicrobial peritonitis suggests intestinal perforation or bowel ischemia. Hepatorenal syndrome is one of the most feared complications of portal hypertension and operative shunting. It is characterized by oliguria, hyponatremia, and low urinary sodium concentration. Patients also exhibit evidence of liver failure such as hyperbilirubinemia and coagulopathy (due to reduced hepatic production of clotting factors). Other causes of renal failure, such as antibiotic induced failure, must be eliminated. Mortality rate approaches 100%, even with aggressive renal dialysis.

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Hemorrhage can be controlled in 90%, although the early rebleeding rate is 30% When medical and surgical treatment are compared, most trials have shown that surgical therapy is better at preventing subsequent bleeding than is medical treatment alone; neither medical or surgical therapy decrease overall mortality rate from portal hypertension, which is directly related to the patients Child classication Except for patients with extremely poor liver function (Child C), patients treated by chronic sclerotherapy have a lower mortality rate than those treated with a portasystemic shunt Encephalopathy aggravated by increased amounts of intestinal protein, regardless of origin; it is worsened by intestinal hemorrhage, constipation, and continued alcoholism Chronic encephalopathy best treated by limitation of protein intake to less than 50 g/day and consumption of a high carbohydrate diet Ascites treated with chronic diuretic administration aimed at reducing the response to aldosterone Complications of shunt placement include peritonitis and DIC; postshunt DIC occurs in up to 50% of patients and evidenced by increased brin split products and decreased platelet count Hepatorenal syndrome one of the most feared complications of portal hypertension and operative shunting; characterized by oliguria, hyponatremia, and low urinary sodium concentration Patients also exhibit evidence of liver failure such as hyperbilirubinemia and coagulopathy (due to reduced hepatic production of clotting factors)

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SUGGESTED READINGS
1. Cello JP et al: Endoscopic sclerotherapy versus portacaval shunt in patients with severe cirrhosis and acute variceal hemorrhage. N Engl J Med 316:11, 1987 An important research study that helped establish sclerotherapy as the standard nonoperative treatment of acute variceal hemorrhage. Although almost 10 years old, it is a classic in the portal hypertension literature and merits close study. 2. Matloff DS: Treatment of acute variceal bleeding. Gastroenterol Clin North Am 21:103, 1992 A good general review of the management of acute variceal hemorrhage. 3. Way LW: Portal hypertension. p. 520. In Way LW (ed): Current Surgical Diagnosis and Treatment. Appleton & Lange, E. Norwalk, CT, 1994 A thorough review of the topic. Contains a very good summary of the surgical management of variceal hemorrhage. An excellent chapter by a world famous authority on the subject.

QUESTIONS 1. The best diagnostic technique to establish the presence of variceal hemorrhage is? A. Angiography. B. Esophagogastroscopy. C. Ultrasonography. D. Contrast radiography. 2. The mortality rate among patients who present with acute variceal hemorrhage is? A. 10%. B. 35%. C. 60%. D. 90%. 3. The best initial measure to control variceal hemorrhage after diagnosis is? A. Sclerotherapy. B. Balloon tamponade. C. Emergency surgery. D. LeVeen Shunt.
(See p. 603 for answers.)