Figure 59-11. Interposition mesocaval shunt. A plastic prosthesis or an autogenous internal jugular vein is used for the shunt. One

end is anastomosed to the inferior vena cava, and the other end is anastomosed to the trunk of the superior mesenteric vein. The

shunt curves around the lower edge of the third portion of the duodenum and is sometimes called a C-shunt.

Advantages to this procedure are the following: (a) control of bleeding is excellent in more than 90%

of patients, (b) no dissection of the porta hepatis is required, (c) hepatopetal flow is maintained, and (d)

the incidence of encephalopathy (5% to 24%) and the risk of progressive liver failure are lower.251

Experience with this shunt has revealed that most patients have hepatopetal flow, with 84% of alcoholic

and 90% of nonalcoholic patients having prograde flow at 4 years after surgery.252 Some loss of

prograde portal flow does occur as a result of either portal vein thrombosis (approximately 10% of

patients) or increased flow through collaterals located along the pancreas. This latter mechanism can be

prevented by complete dissection of the splenic vein from the posterior aspect of the pancreas

(splenopancreatic disconnection),253 but this additional technique adds to the complexity of the

operative procedure and to the incidence of complications.

The distal splenorenal shunt is relatively contraindicated in patients with significant ascites. Because

no portal venous decompression occurs, ascites may increase after a distal splenorenal shunt is created.

In addition, ligation of collateral vessels and lymphatics during the procedure contributes to increased

portal pressures and subsequent increase in ascites. Patients with small splenic veins (<8 mm) have a

relatively high incidence of shunt thrombosis.

Several trials comparing side-to-side total shunts with the distal splenorenal shunt found that they are

equally effective (>90%) in stopping variceal hemorrhage.254 The incidence of hepatic encephalopathy

is lower after the distal splenorenal shunt, with rates of 36% and 15% for the total and selective shunts,

respectively. Rates of rebleeding were similar and ranged from 0% to 30%, with no survival advantage

for either procedure.

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Figure 59-12. Small-diameter interposition portacaval Sarfeh shunt. A vascular prosthesis measuring 8 to 10 mm in diameter is

interposed between the side of the vena cava and the side of the portal vein. The goal is to reduce portal pressure partially and

thereby prevent variceal hemorrhage but still maintain sufficient pressure to permit the prograde flow of portal blood to the liver.

This procedure is simpler to perform than that for the Warren shunt and theoretically avoids the problem of diversion of an

increasing proportion of portal blood away from the liver over time, as occurs with the Warren shunt.

Figure 59-13. Distal splenorenal Warren shunt. The splenic vein is divided near its junction with the superior mesenteric vein. The

distal end of the splenic vein is anastomosed to the renal vein. Varices are selectively decompressed through the stomach and short

gastric veins into the splenic vein and then into the vena cava through the renal vein. Portal hypertension is maintained in the

portal and superior mesenteric veins to provide enough pressure to drive portal blood through the diseased liver.

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Figure 59-14. Transection and reanastomosis of the distal esophagus with the stapling device to control variceal hemorrhage. A: A

stapling device is inserted through a small gastrotomy incision. B: When the device is fired, the esophagus is simultaneously

transected and reanastomosed with staples. C: If the device fires correctly, a complete ring of esophageal tissue is excised.

Investigators have also used the side-to-side nonselective total shunt for the emergency treatment of

bleeding varices. Bleeding stopped in more than 90% of patients with medical therapy alone, although

bleeding often restarted shortly thereafter. Bleeding stopped in all patients after surgery, and 99% of

patients were completely free of episodes of rebleeding. The 5-year survival was approximately 80%,

with the majority of deaths occurring during the first year after surgery as a result of progressive

hepatic failure. Hepatic encephalopathy requiring recurrent intervention, including dietary restriction

and lactulose or neomycin therapy, occurred in 8% of patients. These data support an aggressive,

systematic approach to caring for these patients before, during, and after surgery, though most of these

patients had alcoholic liver disease, which recovers rapidly with withdrawal of the alcohol.

Devascularization Procedures. Devascularization procedures are nonshunting techniques in which the

venous drainage of the stomach and esophagus is disconnected from the liver and intestinal vessels.

These procedures are relatively less technically demanding than shunting procedures and can be

performed in patients with extensive portal thrombosis who preclude other options. They do not

interfere with hepatopetal blood flow and therefore do not increase the incidence of hepatic

encephalopathy.

The procedures range in complexity from simple esophageal transection and reanastomosis with an

end-to-end anastomosis (EEA) stapler combined with ligation of the coronary vein (Fig. 59-14) to the

Sugiura procedure (Fig. 59-15). The Sugiura procedure requires both abdominal and thoracic incisions,

through which a splenectomy, devascularization of the proximal stomach and esophagus, transection of

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the esophagus with reanastomosis, and ligation of all gastroesophageal collaterals are performed.255 The

latter procedure can also be performed via a single abdominal incision.256 Bleeding recurs in fewer than

5% of patients in Japan, but rates of rebleeding range from 10% to 54% in other countries.257 Operative

mortality rates range from 10% to 35% and outcomes are certainly related to the severity of liver

disease. In our practice, these procedures are not used in patients with liver disease, but exclusively in

patients with diffuse portomesenteric thrombosis, in whom decompressive shunts cannot be made.

Figure 59-15. Sugiura esophageal transection and devascularization operation.

Hepatic Transplantation. Liver transplantation is the definitive therapy for portal hypertension and

cirrhosis and the complications thereof, but is indicated for the overall management of end-stage liver

disease and has no role in the control of acute variceal bleeding. When successful, transplantation treats

both the underlying disease and any acute complication.

In conclusion, open surgical intervention short of liver transplantation for patients with cirrhosis and

portal hypertension is becoming a rarity. With the advent of TIPS, the indications for surgically created

shunts are dwindling. Although some studies have shown an increased need for reintervention in

patients who have undergone TIPS for variceal bleeding, the overwhelming efficacy and safety of TIPS

has essentially settled the issue and today, even in large liver centers, open portal decompressive

procedures are rarely performed.

Current guidelines recommend nonselective beta blockade at the maximally tolerated dose for

secondary prophylaxis, followed by serial EVL until all varices are obliterated. Patients should then

undergo surveillance EGD every 6 to 12 months to evaluate for recurrent varices. TIPS should be

reserved for Child A or B patients who bleed again despite combination medical and endoscopic

therapy. Shunt surgery remains an option for good risk Child A patients. Those patients who are

candidates should be referred to a transplant center for timely evaluation.198

Gastropathy and Gastric Varices. Approximately 10% of patients with esophageal varices also have

gastric varices. Conversely, about 90% of patients with gastric varices have esophageal varices.197

Bleeding from gastric varices occurs in approximately 25% of affected patients and is usually more

severe than bleeding from esophageal varices. Rebleeding occurs in up to 30% of patients after an initial

bleed.258 The same pharmacologic interventions used for esophageal varices are used to treat gastric

varices. However, sclerotherapy and EVL have proven relatively ineffective for bleeding gastric varices,

and endoscopic variceal obliteration with tissue adhesives such as N-butyl-cyanoacrylate or isobutyl-2-

cyanoacrylate has shown better rates of initial hemorrhage control and prevention of recurrent

bleeding. A large randomized controlled trial demonstrated better prevention of rebleeding following

acute gastric variceal hemorrhage with N-butyl-cyanoacrylate compared to EVL.259 Balloon tamponade

may also be used as a temporizing measure while arrangements for definitive therapy are made. TIPS is

the primary therapy for controlling gastric varices in patients who fail or cannot receive endoscopic

therapy, with bleeding control rates of over 90% reported.198 The distal splenorenal shunt is reserved

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for the rare patient who cannot receive TIPS.

Portal hypertensive gastropathy is a condition characterized by dilation of the venules and capillaries

of the gastric mucosa without associated inflammation. The major complication of gastropathy is

bleeding; gastropathy accounts for 4% to 38% of all episodes of acute bleeding in patients with

cirrhosis.260 TIPS may provide therapeutic decompression in this setting as well.

Ascites

One of the most important consequences of hepatic dysfunction in cirrhosis and portal hypertension is

ascites. This development portends a significant worsening of the patient’s condition, with markedly

decreased survival rates. Ascites is defined as the accumulation of free fluid within the abdominal cavity

(normally <150 mL). Causes of ascites are listed in Table 59-12. In cirrhosis, the fluid is derived from a

combination of hepatic (high in protein) and splanchnic (low in protein) lymphs that cannot be absorbed

as a result of the increased hydrostatic pressures within the liver and splanchnic systems secondary to

cirrhosis and capillarization of the space of Disse.261 Because of the loss of sinusoidal fenestrations and a

subsequent decrease in their permeability, splanchnic lymph is more abundant than hepatic lymph in

patients with advancing cirrhosis, so that the protein content of ascitic fluid is relatively low.262 The

main underlying pathophysiology in the development of ascites is renal sodium retention and associated

water retention, which lead to fluid overload. Peripheral vasodilation and lower pressures are thought

to be secondary to the dilator effects of nitric oxide, glucagon, and prostaglandins on nascent

arteriovenous shunts present throughout the splanchnic vascular system, as well as in muscle, skin, and

brain. The severity of liver disease is not uniformly correlated with the presence or absence of ascites.

DIAGNOSIS

Table 59-12 Differential Diagnosis of Ascites

Clinical and Laboratory Features. Ascites may be present in patients with cirrhosis who have no other

overt signs or symptoms. Patients may present with subtle signs of weight gain and an inability to fit

into clothes. Physical examination reveals shifting dullness to percussion (1.5 L of ascitic fluid), fluid

waves (10 L), and bulging flanks.263 With progression of disease and massive ascites, respiratory status

may be compromised secondary to increased intra-abdominal pressure and pleural effusions, which are

often present and usually located on the right side. The progression may be slow or more rapid after an

inciting event, such as a variceal bleed or infection.

Stigmata of poor liver function include peripheral muscle wasting, palmar erythema, spider angiomas,

peripheral edema, a palpable liver, and caput medusae (dilated periumbilical veins). With progressive

ascites and increased abdominal pressure, umbilical and inguinal hernias often develop and may be

difficult to manage. Abdominal distention may be caused by gastrointestinal gas rather than ascites. Gas

can be differentiated from fluid by eliciting hyperresonance to percussion, secondary to gas, as opposed

to dullness with fluid. The most widely used test for the diagnosis of ascites is ultrasonography, which

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can also be helpful in determining the best location for therapeutic and diagnostic paracentesis.

Diagnostic Paracentesis. The differential diagnosis of ascites is presented in Table 59-12.

Determination of the character of the ascitic fluid is helpful in establishing the diagnosis. Paracentesis

may be performed in the midline, midway between the umbilicus and the pubic symphysis. The fluid

from patients with cirrhosis is usually straw colored and clear; measurements of protein (usually <2

g/dL), quantitative cell counts, and microbiologic culture and determination of pH, amylase, glucose,

and albumin levels should be obtained. The serum-to-ascitic fluid albumin gradient (SAG) is calculated

by subtracting the albumin concentration in ascites from the level found in serum. This gradient is

helpful in determining the cause of ascites; high values (>1.1 g/dL) are generally associated with portal

hypertension, whereas lower levels may be associated with other disorders, including malignancy.264

Treatment. Initial therapy is usually directed at control of renal sodium and water retention, with bed

rest and dietary manipulation. The upright position exacerbates sodium retention as a result of venous

pooling and relative hypovolemia. Up to 15% of patients respond to this therapy alone with a

natriuresis. A low-sodium diet is a critical part of the management of patients with cirrhosis (1 to 2 g of

sodium per day or 45 to 90 mEq/d). A major problem with a strict low-sodium diet is lack of

palatability and poor compliance. Fluid restriction is also an essential component of therapy in patients

in whom hyponatremia develops (sodium concentration <125 mEq/L), with only 1,000 to 1,500 mL of

fluid allowed each day.

For the 85% to 95% of patients who do not respond to bed rest and fluid and salt restriction, the

mainstay of treatment is diuresis (Table 59-13). The loop diuretic furosemide and the potassium-sparing

diuretic spironolactone are the two most widely used agents, and they can be combined to minimize

side effects and maximize effectiveness. A ratio of 40-mg furosemide to 100-mg spironolactone

generally maintains potassium homeostasis. A diuresis of approximately 500 mL/d is the goal for

patients with mild ascites and of up to 1 to 2 L/d for patients with both ascites and peripheral edema.

More than 90% of patients respond to the combination of dietary manipulation and diuretics.263,265

Complications of the use of spironolactone include painful breast enlargement in males,

hyperkalemia, and metabolic acidosis. Complications of the more potent furosemide include prerenal

azotemia, which occurs in approximately 20% of patients as a result of excessive diuresis and

hypovolemia.274 Additional complications include hyponatremia and encephalopathy.

Large-volume paracentesis (removal of 4 to 6 L of ascitic fluid per day) and total paracentesis are

techniques that can be used for patients with large amounts of fluid who are experiencing symptoms

and are not responding to the aforementioned therapeutic endeavors. Patients requiring paracentesis

usually have severe underlying liver disease and a 1-year survival rate of 25%.266 The technique of

paracentesis involves placing a catheter into the abdominal cavity, either in the lower midline or in one

of the lower quadrants. Care is taken to enter lateral to the rectus muscle and avoid the inferior

epigastric artery. More than 30 L of fluid can be removed by means of total paracentesis, with 6 to 10 g

of albumin infused intravenously for each liter of ascitic fluid removed.263,265,266 The albumin

commonly is administered in the form of 25% albumin (12.5 g/50 mL). Controversy exists regarding

the need for albumin replacement therapy in patients undergoing total paracentesis and repetitive largevolume paracentesis. Patients who have less than 5 L of ascitic fluid removed do not require albumin

replacement.267

TREATMENT

Table 59-13 Treatment of Ascites

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The efficacy of paracentesis in the treatment of tense ascites has been studied extensively. Repetitive

large-volume paracentesis has been shown to be as effective as diuretics in the treatment of moderate to

severe ascites, with fewer systemic complications. A decreased length of hospital stay with no increase

in the incidence of spontaneous bacterial peritonitis has been noted.268 Paracentesis has become the

therapy of choice for severe ascites.

Peritoneovenous shunts are surgically placed tubes that connect the peritoneal cavity with the

superior vena cava via the internal jugular vein (Fig. 59-16). The two main types are the LeVeen shunt

and the Denver shunt, both of which have a one-way valve that allows unidirectional movement of

ascitic fluid from the peritoneal cavity into the systemic circulation. Although these shunts are effective

in decreasing the volume of ascitic fluid, a significant number of major complications have been noted,

including disseminated intravascular coagulation, heart failure, and sepsis,266,269 and associated

mortality rates are high (approximately 20%).270 The shunt is occluded in approximately 50% of

patients at 1 year, and no improvement in survival is noted.266 The use of these shunts has drastically

decreased with the development of the TIPS procedure. In addition to the use of TIPS, the placement of

peritoneovenous shunts is now done percutaneously, further increasing the safety of these procedures.

Surgically created portosystemic shunts have been used in the past for the treatment of ascites.

Because of high morbidity and mortality rates, an increase in encephalopathy and progression to liver

failure, and the addition of the TIPS procedure to treatment options, surgically created shunts are now

used infrequently for this indication alone. As discussed earlier, the TIPS is a total nonselective shunt

that decompresses the portal system and reduces pressure at the hepatic sinusoids, thereby eliminating

the drive for the production of ascitic fluid. In a study evaluating the use of TIPS for the treatment of

medically refractory ascites, the ascites resolved completely in almost 75% of patients, and a partial

response was noted in an additional 20%.271 In addition, renal function improved during the 6 months

of follow-up. TIPS in this group of patients, however, was associated with an increase in the number of

cases of encephalopathy. Although survival appears to be unaffected by a TIPS procedure when

compared with large-volume paracentesis, TIPS may simplify the management of the patient while on

the transplant waiting list.

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