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Review Article

Current Management of Portal Hypertension

Andrew S. Wright, M.D., Layton F. Rikkers, M.D.

Portal hypertension can lead to life-threatening hemorrhage, ascites, and encephalopathy. This paperreviews the pathophysiology and multidisciplinary management of portal hypertension and itscomplications, including the indications for and techniques of the various surgical shunts. Varicealbleeding is the most dreaded complication of portal hypertension. It may occur once the portal-systemicgradient increases above 12 mm Hg, occurs in 30% of patients with cirrhosis, and carries a 30-day

mortality of 20%. Treatment of acute variceal bleeding includes resuscitation followed by upperendoscopy for sclerosis or band ligation of varices, which can control bleeding in up to 85% of patients.

Medical therapies such as vasopressin and somatostatin can also be useful adjuncts. Shunt therapy,preferably the placement of a TIPS, is indicated for refractory acute variceal bleeding. Recurrent varicealbleeding is common and is associated with a high mortality. Therapies to prevent recurrent variceal bleed-ing include chronic endoscopic therapy, nonselective beta-blockade, operative or nonoperative (TIPS)shunts, devascularization operations, and liver transplantation. Recommendations and a treatmentalgorithm are provided, taking into account both the etiology and the manifestations of portalhypertension. ( J GASTROINTEST SURG 2005;9:9921005) 2005 The Society for Surgery of the

Alimentary Tract

KEY WORDS: Portal hypertension, liver, cirrhosis, variceal hemmorhage

Portal hypertension can lead to life-threateningvariceal hemorrhage or development of morbid asci-tes and encephalopathy. In the end stages of portalhypertension secondary to cirrhosis, the hepatore-nal syndrome culminates in kidney and liver failureand carries an extraordinarily high mortality rate.Management of portal hypertension and its attendantcomplications requires a multidisciplinary approachcombining medical and endoscopic management,surgical or nonsurgical portosystemic shunting, and

in some cases liver transplantation.

ETIOLOGY AND PATHOPHYSIOLOGYOF PORTAL HYPERTENSION

Portal hypertension is most often due to increasedportal venous resistance, and is generally classified by

From the Department of Surgery, University of Wisconsin Medical School, Madison, WisconsinReprint requests: Layton F. Rikkers, M.D., H4/710 CSC, University of Wisconsin Hospital and Clinics, 600 Highland Ave., Madison, WI53792. e-mail:[email protected]

2005 The Society for Surgery of the Alimentary Tract 1091-255X/04/$see front matterPublished by Elsevier Inc. doi:10.1016/j.gassur.2004.09.028992

the site of increased resistance as prehepatic, intrahe-patic, or posthepatic (Table 1). The most commoncause of prehepatic portal hypertension is portalvein thrombosis. Isolated splenic vein thrombosiscauses left-sided portal hypertension, usually as aresult of pancreatic inflammation or neoplasm. In thiscase there is venous hypertension of the gastric andsplenic veins with normal portal and superior mesen-teric pressures. Gastric rather than esophageal varicespredominate in this disease because of collateraliza-

tion of the gastroepiploic vein. Isolated left-sidedportal hypertension is reversed by splenectomy alone.Intrahepatic portal hypertension stems from in-

creased vascular resistance at the presinusoidal, sinus-oidal, and/or postsinusoidal levels. The most commoncause of presinusoidal portal hypertension is schistoso-miasis. Nonalcoholic cirrhosis may also cause presi-nusoidal portal hypertension, especially early in the
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Vol. 9, No. 72005 Current Management of Portal Hypertension 993

Table 1.Classification of portal hypertension

ExtrahepaticPortal vein thrombosisSplenic vein thrombosis

Intrahepatic

PresinusoidalSchistosomiasisPrimary biliary cirrhosisSarcoidosisMyeloproliferative disease (Hodgkins disease,

myelogeneous leukemia)Gauchers diseaseCongenital hepatic fibrosisArsenic toxicity

SinusoidalAlcoholic cirrhosisStorage diseasesHemochromatosisWilsons disease

PostsinusoidalAlcoholic cirrhosisVeno-occlusive disease

PosthepaticBudd-Chiari syndromeRight-sided heart failureConstrictive pericarditis

High-flow portal hypertensionHepatic arteryportal vein fistulaSplenic arteriovenous fistulaMassive splenomegaly

course of the disease. Sinusoidal portalhypertension ismost often due to alcoholic cirrhosis, with depositionof collagen in the space of Disse. Alcoholic cirrhosismay also cause increased postsinusoidal resistanceas regenerating nodules compress small hepatic veins.

Postsinusoidal syndromes are rare, but include Budd-Chiari syndrome (thrombosis of hepatic veins), rightheart failure, and constrictive pericarditis. Portal hyper-tension may rarely be caused by increased portal venousflow alone, due to either massive splenomegaly or asplanchnic arteriovenous malformation.

PATHOPHYSIOLOGY AND PROGNOSISOF ACUTE VARICEAL HEMORRHAGE

Portal hypertension is characterized by a gradientof greater than 5 mm Hg between the portal venousand central venous pressures. After a pressure gradi-ent of 8 to 10 mm Hg is reached, esophageal andgastric varices arise from a collateral network throughthe coronary and short gastric veins into the azygousvein. Bleeding canoccur once the gradient increasesabove 12 mm Hg.1,2 Other sites of collateralization

include retroperitoneal vessels, the hemorrhoidalvenous plexus, a recanalized umbilical vein, and intra-hepatic shunts.

Esophageal varices are common in cirrhotic pa-tients and frequently progress over time. In one longi-tudinal series, new varices arose in 5% of cirrhotic

patientswithin 1 year and in 28% of patients within3 years.3 Progression was predicted by Child-Pughscore, the presence of red wale markings on the vari-ces, and an alcoholic etiology of cirrhosis. In patientswith small varices at initial endoscopy, the 2-year riskof variceal bleeding is 12%. Thirty-day mortality ofvariceal bleeding ranges from 20% to 29%.4

The pathogenesis of variceal rupture is related tophysical factors within the wall of the varix. Portalpressure, variceal size, and epithelial thickness all con-tribute to the likelihoodof variceal rupture as relatedby the law of Laplace.5 The risk of bleeding is inde-

pendently associated withvarix size for both esopha-geal6 and gastric varices.7 Physical appearance canalso predict bleeding, including red wale markings,cherryred spots, hemocytic spots, and diffuse ery-thema.3,7,8 Location of varices is important, with iso-lated gastric varices being more likely to bleed andhaving a greater transfusion requirement than esoph-ageal varices.8

Over 90% of active gastrointestinal hemorrhages inthesetting of portal hypertension are caused by vari-ces,6 but bleeding may also stem from peptic ulcerdisease, Mallory-Weiss tears, or gastric antral vascu-lar ectasia. Portal hypertensive gastropathy (PHG) isan additional nonvariceal source of upper gastroin-testinal bleeding in patients with portal hyper-tension.9 The frequency is unknown but seems toincrease after endoscopic treatment of esophagealvarices. PHG consists of erythematous areas of thegastric fundus and body that are enclosed by awhite reticular network. The appearance of granularmucosa with cherry-red spots indicates a more severeform of PHG and a higher risk of rebleeding.

Acute variceal bleeding has a mortality of 25% to30%, accounts for one-third of deaths among patientswith cirrhosis, and occurs in 25% to 40% of pa-

tients with cirrhosis.10 Risk of death is related to theunderlying hepatic functional reserve. About half ofpatients will stop bleeding following resuscitationalone.11 Spontaneous cessation of hemorrhage is lesslikely in patients with Child-Pugh classC cirrhosis orwith large, actively spurting varices.12

Rebleeding is common following variceal hemor-rhage. More than 50% of all recurrent bleedingoccurs within the first 10 days, with a period of great-est risk within the first 72 hours. Risk factors forearly rebleeding include large varices, severe initialbleeding (hemoglobin 8 g/dl), renal failure, and


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Journal ofGastrointestinal Surgery994 Wright and Rikkers

age more than 60 years.13 After6 weeks the risk ofrebleeding returns to baseline.14

PROPHYLACTIC THERAPY

Because of the high mortality and morbidity ofvariceal bleeding, primary prevention of bleeding is amajor goal in the management of portal hypertension.Nonselective beta-blockers such as propranolol andnadolol reduce portal venous inflow by blockingadrenergic dilatation of mesenteric arterioles. Beta-blockers reduce the risk of first variceal bleeding by45% to 50% compared to placebo; however, a survivaladvantage has not been demonstrated.15,16 Nitratesalso reduce portal pressure and have been comparedto beta-blockers in several trials. Although bleedingrates appear to be similar, long-term survival ratesare lower in patients receiving nitrates.17 Results with

combination therapy have been inconclusive.18,19Throughout the late 1960s and early 1970s, several

groups investigated use of the portacaval shunt forprevention of variceal bleeding. Although surgery washighly successful in reducing the incidence of bleed-ing, encephalopathy was frequent, and there was asurvival benefit to medical therapy.2022There are nodata regarding the transjugular intrahepatic portosys-temic shunt (TIPS) in the prevention of primary vari-ceal bleeding, and it is not currently recommendedfor this purpose. Some early reports recommendsclerotherapy for prophylaxis of primary variceal

bleeding,23

but more recent studies show no benefit16

or higher mortality in groups receiving sclerother-apy.24A meta-analysis comparing esophageal bandingand beta-blockers showed decreased risk of bleed-ing with banding but no difference in mortality.25

Recurrence of varices is high, and banding is currentlyrecommended only for patients who are at high riskof bleeding and who cannot tolerate beta-blockers.

MEDICAL AND ENDOSCOPICMANAGEMENT OF ACUTEVARICEAL BLEEDING

A patient with suspected variceal bleeding mustfirst be appropriately resuscitated and hemodynami-cally stabilized. The stomach should be evacuatedwith a large-bore gastric lavage tube. Transfusionsof blood, and when appropriate fresh frozen plasma,should be used to restore adequate blood volumeand correct coagulopathy. Platelet counts often dropwithin the 48 hours following an acute bleed, andplatelets should be transfused as necessary. Correc-tion of coagulopathy may not be successful with freshfrozen plasma alone. In a small pilot study, 10 patients

with active variceal bleeding were given a single doseof recombinant human factor VIIa. Prothrombintime normalized in all patients within 30 minutes,with immediate control of bleeding.26

Patients with acute variceal bleeding are at riskof serious morbidity due to decompensated hepatic

function, encephalopathy, coagulopathy, and poornutrition. Primary bacterial infections are present in20% of cirrhotic patients with gastrointestinal bleed-ing, and secondary infections may occur in up to50%.27 A meta-analysis of more than 800 patientsshowed a reduction in mortality with administrationof prophylactic antibiotics.28 There is no consensusregarding the antibiotic regimen of choice.

Endoscopy should be performed as soon as thepatient is resuscitated. Band ligation and sclerother-apy control bleeding in more than 85% of patients(Fig. 1).29,30A meta-analysis comparing band ligationwith sclerotherapyfound lower rebleeding and mor-tality with ligation.31 Band ligation, however, is tech-nically more difficult, and either treatment option isconsidered acceptable.

After endoscopic treatment, a repeat endoscopyshould be planned in 4 to 6 days. Minor complica-tions are common, including chest pain, ulceration,and fever. Major complications include perforation,hemorrhage, aspiration, and late stricture formation.These complications are less frequent followingbanding compared to sclerotherapy. Mortality sec-ondary to the procedure ranges from 1% to 3%.Endoscopic therapy should be considered a failure if

hemorrhage is not controlled after two sessions, atwhich point mortality increases to 60% withoutfurther intervention.

Vasopressin is a splanchnic vasoconstrictor thatreduces portal flow and portal pressure. Vasopressincontrols acute hemorrhage in up to 60% of patients,but has limited efficacy in preventing early rebleedingand does not improve survival. It has been shown inameta-analysis to be more effective than placebo.29

Vasopressin should be used in an intensive care set-ting because of its side effects, including hypertension,bradycardia, coronary vasoconstriction, and decreasedcardiac output. Vasopressin is usually administered as

a bolus of 0.4 units, followed by a drip at a rate of0.4 to 1 units per minute. Nitroglycerin, given incombination with vasopressin, enhances reductionin portal pressure while counteracting systemicvasoconstriction. Combined therapy results in morefrequent cessation of bleeding (68% vs. 44%) andreduced morbidity (3% vs. 21%) compared tovasopressin alone.32

Somatostatin and its analog, octreotide, indirectlydecrease portal flow by inhibiting the vasodilatory ef-fects of glucagon. A meta-analysis comparing somato-statin to vasopressin found better bleeding control and


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Fig. 1.Techniques of (A) sclerotherapy and (B) endoscopic band ligation. (Adapted from Marvin MR,Emond JC. Cirrhosis andportal hypertension. In Greenfield LJ, Mulholland MW,Oldham KT,Zelenock

GB, Lillemoe KD, eds. Surgery: Scientific Principles and Practice, 3rd ed. Philadelphia: LippincottWilliams & Wilkins, 2001, p 971.) Reprinted with permission.

fewer adverse effects (0% vs. 10%) with somatostatin.33

Compared with sclerotherapy, both somatostatin34

and octreotide35 have equivalent rates of bleedingcontrol, early rebleeding, and mortality. Combina-tion of somatostatin or octreotide with sclerotherapyappears to be more effective thandrugtherapy, scler-otherapy, or band ligation alone.3638

In patients with life-threatening bleeding thatcannot be successfully stopped by endoscopy, balloon

tamponade can be used as a temporizing measure(Fig. 2). The Sengstaken-Blakemore tube stopsacute variceal bleeding in up to 85% of patients, butthe risk of recurrent hemorrhage following deflationis up to 50%.39 The device is uncomfortable for thepatient and carries a 14% risk of serious complica-tions. Intraesophageal inflation of the gastric ballooncan result in esophageal perforation, while ischemicnecrosis of the esophagus can occur because of over-inflation of the esophageal balloon. Complicationsappear to be more commonwhen balloons are placedby inexperienced personnel.39 Because of the high risk

of rebleeding, definitive therapy should be planned inall patients treated with balloon tamponade.

SHUNT THERAPY IN THEMANAGEMENT OF ACUTEVARICEAL BLEEDING

With failure of endoscopic and pharmacologictherapy, the portal system should be decompressedvia a shunt between the portal and systemic venouscirculations. Shunting of portal blood, however, may

result in adverse effects due to diversion of hormones,nutrients, and toxins around the liver, leading toencephalopathy and accelerated hepatic failure.

In most institutions the transjugular intrahepaticportosystemic shunt (TIPS) has become the emergentshunt procedure of choice. After the internal jugularvein is accessed, a wire is threaded into a hepatic veinand then punctured throughthe liver into a branchof the portal system (Fig. 3). A tract is developed

using a balloon dilator, and an expandable metal stentis inserted to maintain patency of the shunt. TIPSplacement requires an expert interventional radiolo-gist and may not be available in all centers. BecauseTIPS completely diverts portal flow, it is considereda nonselective shunt.

TIPS achieves hemostasis in the majority of pa-tientswith bleeding refractory to endoscopic manage-ment.40,41 In patients with refractory bleeding whoare at prohibitive riskfor emergent surgery (because ofsepsis, coma, multisystem organ failure, or severecomorbidities), TIPS is successful at achievinghemostasis in 90%, with a 63% 30-day survival.42

TIPS may also be useful in patients with severe he-patic dysfunction (i.e., Child-Pugh class C), who maynot be well served by emergency operation.

TIPS is especially useful as a short-term bridge toliver transplantation, because the TIPS proceduredoes not disturb the anatomy of the liver or portaltriad. A lower portal pressure may make transplanta-tion technically easier. Absolute contraindications toTIPS are polycystic liver disease and right heart fail-ure, while relative contraindications include portalvein thrombosis, hypervascular liver tumors, andencephalopathy.


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Fig. 2.The Sengstaken-Blakemore tube, used to tamponadebleeding gastroesophageal varices. Patients should also be en-dotracheally intubated to protect the airway. (Adapted fromMarvin MR, Emond JC: Cirrhosis and portal hypertension.In Greenfield LJ, Mulholland MW, Oldham KT, ZelenockGB, Lillemoe KD, eds. Surgery: Scientific Principles and Prac-tice, 3rd ed. Philadelphia: Lippincott Williams & Wilkins,2001, p 972.) Reprinted with permission.

Urgent or emergent surgery is required when en-doscopic and pharmacologic therapies are unsuccess-ful and TIPS placement is contraindicated,unavailable, or unsuccessful. Orloff and colleagueshave reported 99% success in control of acute varicealbleeding with the portacaval shunt in 400 patients.43

Although 30-day survival was only 58% in the first15 years of the series, survival increased to 85% inthe final 12 years. In the latter group, 5-year survivalwas 78%. Encephalopathy occurred in only 9% of

patients. It should be noted, however, that no oneelse has been able to duplicate the results of thissingle-center experience.

MEDICAL AND ENDOSCOPIC THERAPYIN THE PREVENTION OF RECURRENTVARICEAL BLEEDING

Recurrence of variceal bleeding is common andoccurs in up to 70% of patients following medicaland endoscopic management.44 Mortality in the first

year following variceal hemorrhage is as high as 70%in untreated patients, due to recurrent bleeding, liverfailure, and infections. Prevention of rebleeding andpreservation of liver function are therefore the twolong-term goals of therapy.

Chronic endoscopic therapy is currently the most

common means for long-term prevention of recur-rent variceal bleeding. Compared to medical treat-ment, sclerotherapy decreases 40-day mortality by43%.45 Repeat sclerotherapy can eradicate varices in88% of patients surviving longer than 3 months, butvarices eventually recur in most of these patients.46

A meta-analysis has shown endoscopic band ligationto be superior to sclerotherapy, with less rebleed-ing, death, and esophageal stricture formation.47

Fewer treatments are required to eradicate variceswith band ligation. The combination of sclerotherapyand band ligation appears to decrease efficacy and

increase complication rates, and is therefore notrecommended.Just as propranolol has been shown to be effective

prophylaxis against initial episodes of variceal hemor-rhage, it is also useful in prevention of recurrentbleeding. The risk of recurrent bleedingis lessenedbyabout 40%,and the risk ofdeath by20%.48 Combi-nation therapy with a beta-blocker and a long-actingnitrate is probably more effective than beta-blockadealone.49 A response to medical therapy, as indicatedby a reduction in hepatic venous pressure gradientor measuredvariceal pressure, predicts a lower riskof rebleeding.50

Pharmacologic therapy with propranolol is proba-bly somewhat less effective than endoscopic manage-ment, with one meta-analysis finding 45% of patientsrebleeding with sclerotherapy compared to 61% withmedical managment.29A combination of nadolol andisosorbide mononitrate has been shown to be moresuccessful than endoscopic ligation (33% vs. 49%rebleeding), with better efficacy in patients with a he-modynamic response to medication.52 Because of therisk of rebleeding, long-term pharmacotherapy shouldbe used only in compliant patients with close physicianmonitoring. There appears to be no added benefit with

combined beta-blockade and sclerotherapy.53

SHUNT THERAPY IN THE PREVENTIONOF RECURRENT VARICEAL BLEEDING

Both nonoperative and surgical shunts play a rolein the prevention of recurrent variceal bleeding.Portosystemic shunts are classified as nonselective,selective, and partial, depending on howmuch hepaticportal flow is preserved. Nonselective shunts decom-press the entire portal system by diverting all portal


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Fig. 3.Technique for placement of a transjugular intrahepatic portasystemic shunt (TIPS). A needle isplaced from the hepatic into the portal vein via a transjugular approach. A guidewire is then advanced

and used to dilate a tract and place an expandable stent. (Adapted from Zemel G, Katzen BT, BeckerGJ, Benenati JF, Sallee DS. Percutaneous transjugular portosystemic shunt. JAMA 1991;266:390.) Copy-righted1991 American Medical Association. All rights reserved.

blood flow. Selective shunts attempt to decompressonly the variceal-bearing compartment of the portalvenous system while preserving some portal flow tothe liver. Partial shunts, in contrast, incompletelydecompress the portal system and maintain someportal flow.

Non-selective shunts include TIPS, the Eck fistula

(end-to-side portacaval shunt), the side-to-side por-tacaval shunt, interposition shunts, and the conven-tional splenorenal shunt(Fig. 4). Numerous studieshave compared TIPS with endoscopic managementin prevention of recurrent bleeding. Although TIPSreduced the rate of rebleeding in a meta-analysis of811 patients, overall survival was unchanged and therate of encephalopathy was increased.54The primaryreasons for recurrence of bleeding following TIPSare shunt thrombosis and stenosis, which occur inover 50% of patients within the first 2 years.55 Al-though these problems may be managed by balloon

dilatation or placement of a second shunt, there isrelatively little data regarding long-term shunt pat-ency. Because of frequent shunt failure, many patientsrequire multiple interventions over time. In mostseries, both the number of interventions and overallcosts are higher following TIPS compared to endo-scopic therapy.56 TIPS is therefore recommendedonly as salvage therapy in patients failing medicaland endoscopic therapy.42

The end-to-side portacaval shunt has been com-pared to medical therapy in 4 randomized trials, noneof which demonstrated a difference in survival.29All ofthe studies had a crossover bias in favor of medicalmanagement, because some patients received shuntsfor failure of medical therapy. Shunted patients hadexcellent control of bleeding, but encephalopathy wassevere in up to 40% of patients. Although bleedingwas the most common cause of death in medically


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Fig. 4. Nonselective portasystemic shunts: (A) the end-to-side portacaval shunt (Eck Fistula), (B) theside-to-side portacaval shunt, and (C) the interposition mesocaval shunt. (Adapted from Marvin MR,Emond JC. Cirrhosis and portal hypertension. In Greenfield LJ, Mulholland MW,Oldham KT, ZelenockGB, Lillemoe KD, eds. Surgery: Scientific Principles and Practice, 3rd ed. Philadelphia: LippincottWilliams & Wilkins, 2001, pp 974975.) Reprinted with permission.

managed patients, accelerated hepatic failure was theleading cause of mortality following operative shunting.

The distal splenorenal shunt is considered to be aselective shunt because it can preserve superior mes-enteric blood flow to the liver. The distal splenorenalshunt includes an anastomosis of the distal splenicvein to the renal vein and interruption of all collateralvessels connecting the superior mesenteric and gas-trosplenic components of the portal system (Fig. 5).This leaves a decompressed gastrosplenic circuit anda high-pressure superior mesenteric circuit that con-tinues to perfuse the liver. Ascites may be worsenedby the distal splenorenal shunt, as mesenteric venoushypertension continues and retroperitoneal lymphat-ics are disrupted. A small diameter splenic vein (7mm) is a relative contraindication to the distal splen-orenal shunt because of a high incidence of shuntthrombosis.

Collateralization between circuits following thedistal splenorenal shunt leads to a loss of portal flowin approximately 50% of patients by 1 year. Thisoccurs primarily in patients with alcoholic cirrho-sis, while portal flow seems to be better maintained inpatients with nonalcoholic cirrhosis and noncirrhoticportal hypertension.57 Failure to ligate the coronaryvein leads to rapid collateralization. Collaterals mayalso form through the pancreas (pancreatic siphon).This can be prevented by splenopancreatic discon-nection, which consists of dissecting the full lengthof the splenic vein from the pancreas. This procedure,

however, adds considerably to the technical difficultyof the operation.

There have been several controlled studies com-paring the distal splenorenal shunt to nonselectiveshunts, none of which have demonstrated a survivaladvantage for either type of procedure.58 Among pa-

tients with presinusoidal portal hypertension, enceph-alopathy is reduced following selective as opposed tononselective shunting.59 Of note, six of the seven con-trolled studies included a preponderance of alcoholiccirrhotics. Three of these have shown a decreasedrate of encephalopathy following the selective shunt.Because encephalopathy appears to be less followingthe selective shunt, it can be recommended even inalcoholic patients.60 Survival after the distal splenorenalshunt maybe higher among those with nonalcoholiccirrhosis,61 perhaps because of better preservation ofhepatic portal perfusion.

In a meta-analysis of 4 trials comparing the distalsplenorenal shunt and sclerotherapy, the relativeriskof rebleeding was 0.16 with surgical shunting.62 Nei-ther survival nor encephalopathy was significantly dif-ferent betweenthetwointerventions. Thesettings ofthefour studies were different, perhaps obscuring somedifferences between sclerotherapy and shunting. In amajor metropolitan center, survival was significantlybetterwith sclerotherapy than the distal splenorenalshunt.63Thirty-five percent of sclerotherapy patientsrequired surgical rescue, and 85% of these patientswere successfully salvaged. On the other hand, sur-vival in a more rural setting was significantly better


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Fig. 5. The distal splenorenal shunt. (From Salam AA. Distal splenorenal shunts: Hemodynamics oftotal versus selective shunting. In Baker RJ, Fischer JE, eds. Mastery of Surgery, 4th ed. Philadelphia:Lippincott Williams & Wilkins, 2001, pp 13571366.) Reprinted with permission.

following surgery (53%6-year survival, compared to26% for sclerotherapy).64 In this study only 31% ofsclerotherapy failures were able to be salvaged witha surgical shunt. Given these disparate findings, areasonable approach is endoscopic therapy with sal-vage shunting in patients with ready access to medi-cal care. Primary shunting may be beneficial in ruralareas or in patients unlikely to be compliant withongoing medical management.

Like selective shunts, partial shunts aim to decom-press varices while maintaining hepatic portal flow.Most small-diameter venous partial shunts eitherthrombose or dilate over time, thereby becomingnonselective. A small diameter polytetrafluoroethy-lene (PFTE) shunt, when combined with coronaryvein ligation and division of collaterals, provides afixed resistance and is more likely to maintain hepato-petal portal flow (Fig. 6).65 Compared with larger,

nonselective portocaval interposition shunts, thesmaller (8 mm) PTFE shunt is followed by improvedsurvival and less encephalopathy in some studies.66,67

The choice of surgical shunting versus TIPS is stillin question. A randomized trial comparing TIPS andan 8 mm H-type portacaval prosthetic shunt found alower failure rate with surgical shunting.68 Rebleed-ing, liver transplantation, and late death were morefrequent following TIPS. A separate, nonrandomizedseries found that rebleeding, encephalopathy, andshunt thrombosis are less but ascites is worse follow-ing a distal splenorenal shunt compared to TIPS.69

In a decision-analysis economic model, the distalsplenorenal shunt was significantly less expensive thanTIPS, with fewer procedures required.70A multicenterrandomized trial comparing TIPS with the distalsplenorenal shunt is ongoing.

NONSHUNT SURGICAL THERAPY INTHE PREVENTION OF RECURRENTVARICEAL BLEEDING

There are a number of nonshunt surgical alterna-tives for the management of variceal bleeding. Simpleesophageal transection is as effective as sclerotherapy,but variceal recurrence and rebleeding are common.71

The Sugiura procedure (esophagogastric devasculari-zation with splenectomy and preservation of the coro-nary and para-esophageal veins) had a rebleedingrateof less than 10% in a Japanese series (Fig. 7).72,73

Modifications of this procedure have not been as suc-cessful in North America, likely due to a differenceinthe proportion of patients with alcoholic cirrho-sis.74 The Sugiura procedure is especially useful forpatients who are unable to undergo shunting becauseof extensive portal, splenic, and superior mesentericvein thrombosis.

LIVER TRANSPLANTATION

Liver transplantation is the only therapy that ad-dresses both portal hypertension and the underlying


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Fig. 6.The small-diameter diameter portacaval H graft inter-position (partial) shunt. (From Sarfeh IJ, Rypins EB, MasonGR: A systematic appraisal of portacaval H-graft diameters:Clinical and hemodynamic perspectives. Ann Surg1986;204:356363.) Reprinted with permission.

liver disease. About 6000 liver transplants are per-formed annually in the United States, far more thanthe number of surgical shunts. Transplantationshouldbe a considerationin allpatients with end-stageliver failure. At the University of Wisconsin overallpatient survival following liver transplantation is89%, 79%, and 74% at 1, 3, and 5 years respectively.Transplant is most appropriate for patients with non-alcoholic cirrhosis or abstinent patients with alco-holic cirrhosis.

Shunt surgery may be used as a bridge to transplantin selected patients. In a series of 77 patients receivinga surgical shunt,44were considered eligible for laterliver transplant.75 Seven of these ultimately un-derwent transplantation, and only two died of liverfailure without transplant. Survival of the transplantcandidates who underwent a distal splenorenalshunt with transplantation as a salvage therapy wassignificantly better than that of patients receiving atransplant without a prior shunt operation.

In patients with a previous portasystemic shunt,the shunt should be taken down at the time oftransplant surgery to preserve hepatic blood flow.Ligation of a distal splenorenal shunt is more difficult,and can best be managed via splenectomy or ligationof the renal vein.

ASCITES

Development of ascites is a sign of progressiveliver dysfunction, and portends a worsening progno-sis. Two-year survival with controlled ascites is50%,76 but mortality of patients with refractoryasci-

tes is 50% at 6 months and 75% at 1 year.77

Withdevelopment of the hepatorenal syndrome,mortalityapproaches 100% without liver transplant.78

Development of ascites is due to an imbalance innet capillary permeability and hydraulic and oncoticpressure gradients. Ascites does not occur until theportal-systemic pressure gradient is greater than 12mm Hg,79 and disappears if thegradient falls below12 mm Hg following shunting.80 Ascites was oncethought to be primarily due to obstruction of portalvenous outflow. Animal models and in vivo humandata, however, suggest that increased portal inflow ismore important. This increase in portal flow is due tonitric oxidemediated vasodilatation of the splanchnicbed. Chronic vasodilatation activates the renin-aldosterone system, leading to sodium retention bythe kidneys.

If possible the underlying source of cirrhosis shouldbe treated. Ascites related to alcoholic cirrhosis willimprove with abstinence,81 while patients with auto-immune hepatitis may improve with steroid therapy.Salt restriction and diuretic therapy are the mainstaysof medical therapy for ascites. Dietary changes alone(usually a limit of 2000 mg of sodium per day)are effective in only a small subset of patients. Spiro-

nolactone is the first-line diuretic of choice, as it is analdosterone antagonist. The addition of furosemide,although not confirmed in randomized trials, isthought to prevent hyperkalemia. The initial goal ofdiuretic therapy should be a weight loss of approxi-mately 1 pound per day. Patients refractory to medicaltherapy require more aggressive intervention, oftenincluding large-volume paracentesis with or withoutalbumin infusion.82,83

TIPS is effective in 80% of patients with medicallyintractable ascites, butcarries the risk of encephalopa-thy in 30% of patients.84 Although ascites appears to

be better controlled with TIPSthan serial paracente-sis, survival is not improved.85 Surgical portasystemicshunting is occasionally indicated for patients withascites and variceal bleeding who fail TIPS. Perito-neovenous shunts are rarely indicated; they have ahigh rate of infection and thrombosis andmay lead todisseminated intravascular coagulation.86 In a recentprospective randomized trial, control of ascites andoverall survival were significantly better followingTIPS compared to peritoneovenous shunting.87 Livertransplantation should be considered when ascitescomplicates chronic liver disease.


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Fig. 7. Esophageal transection with esophagogastric devascularization (Sugiura procedure). (Modifiedfrom Sugiura M, Futagawa S: Further evaluation of the Sugiura procedure in the treatment of esophagealvarices. Arch Surg 1977;112:1317.)Copyrighted 1991 American Medical Association.All rights reserved.

RECOMMENDATIONS

Treatment of variceal bleeding and portal hyper-tension has changed markedly over the last 30 yearswith the development of endoscopic therapies, im-proved medical management, liver transplantation,and TIPS. Management of acute variceal bleedingbegins with adequate resuscitation and correctionof coagulopathy followed by endoscopic control ofbleeding. Band ligation is more successful but alsomore technically demanding than sclerotherapy, andeither technique is acceptable. Medical therapy withvasopressin and nitroglycerin or with octreotide isalso useful, with a combination of octreotide and en-

doscopic therapy being the most effective. Antibioticsshould be given during an episode of variceal bleedingto prevent secondary complications. With failure ofmedical and endoscopic surgery, emergent nonopera-tive or surgical shunting should be considered.

Long-term management of varices now relies onthe relative appropriateness of liver transplantation.Suitable patients with decompensated hepatic func-tion (Child-Pugh classes B and C) or a poor qualityof life secondary to liver disease should undergo trans-plantation as soon as possible. If a transplant is notreadily available, or if a patient is not suitable for

transplant, medical and endoscopic therapy should

be the first line of treatment.Good risk (Child-Pugh classes A and B) patients

with refractory variceal bleeding despite pharmaco-therapy and/or endoscopic therapy should receive aselective shunt or small diameter PTFE partial shunt.Operative shunting is also indicated as primary ther-apy for noncompliant patients and for patients wholive in remote areas. Data comparing TIPS and surgi-cal shunting in this patient population are not yetavailable. Although TIPS has replaced surgicalshunting in many institutions, the distal splenore-nal shunt has better patency and less rebleeding.

Nonselective shunting (TIPS or side-to-side porto-systemic shunt) is indicated for patients with intracta-ble ascites and variceal bleeding. TIPS is especiallyindicated for patients with failure of endoscopic ther-apy who may be transplant candidates in the nearfuture and for poor risk (Child-Pugh class C) non-transplant candidates (e.g., active alcoholics) who areunlikely to outlive their TIPS. A recommended treat-ment algorithm for variceal bleeding is shown inFig. 8.

Ascites carries high morbidity and mortality. Initialtreatment consists of managing the underlying cause


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Fig. 8. Recommended treatment algorithm for definitive therapy of variceal bleeding. (From RikkersLF. Surgical complications of cirrhosis and portal hypertension. In Townsend CM Jr, ed. SabistonTextbook of Surgery, 17th ed. Philadelphia: Elsevier; 2004. p. 1592.) Reprinted with permission.

of cirrhosis. Salt restriction alone (2000 mg/day)is successful in only a small number of patients. Acombination of spironolactone and furosemide im-proves ascites by targeting the renin-aldosteronesystem while preventing hypokalemia. With failure ofmedical therapy, both large-volume paracentesis andTIPS are useful. Liver transplantation should be con-sidered in all patients with chronic liver disease andascites.

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