Surgery (Portal Hypertension)

1. THE KURSK STATE MEDICAL UNIVERSITY
DEPARTMENT OF SURGICAL DISEASES № 1
PORTAL HYPERTENSION
Information for self-training of English-speaking students
The chair of surgical diseases N 1 (Chair-head - prof. S.V.Ivanov)
BY ASS. PROFESSOR I.S. IVANOV
KURSK-2010

2. Portal hypertension
Introduction:
Background: Portal hypertension may be defined as a portal pressure gradient of 12
mm Hg or greater and is often associated with varices and ascites. Many conditions are
associated with portal hypertension, of which cirrhosis is the most common cause.
The portal vein drains blood from the small and large intestines, stomach, spleen,
pancreas, and gallbladder. The superior mesenteric vein and the splenic vein unite
behind the neck of the pancreas to form the portal vein. The portal trunk divides into 2
lobar veins. The right branch drains the cystic vein, and the left branch receives the
umbilical and paraumbilical veins that enlarge to form umbilical varices in portal
hypertension. The coronary vein, which runs along the lesser curvature of the stomach,
receives distal esophageal veins, which also enlarge in portal hypertension.
Pathophysiology: Two important factors exist in the pathophysiology of portal
hypertension, vascular resistance and blood flow. Ohm law is V = IR, where V is
voltage, I is current, and R is resistance. This can be applied to vascular flow, ie, P = FR,
where P is the pressure gradient through the portal venous system, F is the volume of
blood flowing through the system, and R is the resistance to flow. Changes in either F or
R affect the pressure. In most types of portal hypertension, both the blood flow and the
resistance to blood flow are altered.
Increase in vascular resistance
The initial factor in the pathophysiology of portal hypertension is the increase in
vascular resistance to the portal blood flow. Poiseuille law, which can be applied to
portal vascular resistance, states that R = 8L/r4
, where  is the viscosity of blood, L
is the length of the blood vessel, and r is the radius of the blood vessel. The viscosity of
the blood is related to the hematocrit (HCT). The lengths of the blood vessels in the
portal vasculature are relatively constant. Thus, changes in portal vascular resistance are
determined primarily by blood vessel radius. Because portal vascular resistance is
indirectly proportional to the fourth power of the vessel radius, small decreases in the
vessel radius cause large increases in portal vascular resistance and, therefore, in portal
blood pressure (P = F8L/r4
, where P is portal pressure and F is portal blood flow).
Liver disease is responsible for a decrease in portal vascular radius, producing a
dramatic increase in portal vascular resistance. In cirrhosis, the increase occurs at the
hepatic microcirculation (sinusoidal portal hypertension). Increased hepatic vascular
resistance in cirrhosis is not only a mechanical consequence of the hepatic architectural
disorder, but a dynamic component also exists due to the active contraction of
myofibroblasts, activated stellate cells, and vascular smooth-muscle cells of the
intrahepatic veins.

3. Endogenous factors and pharmacological agents that modify the dynamic component
include those that increase hepatic vascular resistance and those that decrease hepatic
vascular resistance. Factors that increase hepatic vascular resistance include endothelin,
alpha-adrenergic stimulus, and angiotensin II. Factors that decrease hepatic vascular
resistance include nitric oxide, prostacyclin, and vasodilating drugs (eg, organic nitrates,
adrenolytics, calcium channel blockers).
Increase in portal blood flow
The second factor that contributes to the pathogenesis of portal hypertension is the
increase in blood flow in the portal veins, which is established through splanchnic
arteriolar vasodilatation caused by an excessive release of endogenous vasodilators (eg,
endothelial, neural, humoral). The increase in portal blood flow aggravates the increase
in portal pressure and contributes to why portal hypertension exists despite the formation
of an extensive network of portosystemic collaterals that may divert as much as 80% of
portal blood flow.
Manifestations of splanchnic vasodilatation include increased cardiac output, arterial
hypotension, and hypervolemia. This explains the rationale for treating portal
hypertension with a low-sodium diet and diuretics to attenuate the hyperkinetic state.
Frequency:
• In the US: Incidence is not known.
• Internationally: Incidence is not known.
Mortality/Morbidity: Variceal hemorrhage is the most common complication
associated with portal hypertension. Almost 90% of patients with cirrhosis develop
varices, and approximately 30% of varices bleed. The first episode of variceal
hemorrhage is estimated to carry a mortality rate of 30-50%.
Clinical:
History: The medical history from a patient with portal hypertension should be directed
towards determining the cause of portal hypertension and, secondarily, the presence of
the complications of portal hypertension.
• Determining the cause of portal hypertension involves the following:
o History of jaundice
o History of blood transfusions, intravenous drug use (hepatitis B and C)
o Pruritus

4. o Family history of hereditary liver disease (hemochromatosis, Wilson
disease)
o History of alcohol abuse
• Determining the presence of the complications of portal hypertension involves the
following:
o Hematemesis or melena (gastroesophageal variceal bleeding or bleeding
from portal gastropathy)
o Mental status changes such as lethargy, increased irritability, and altered
sleep patterns (presence of portosystemic encephalopathy)
o Increasing abdominal girth (ascites formation)
o Abdominal pain and fever (spontaneous bacterial peritonitis [SBP], which
also presents without symptoms)
o Hematochezia (bleeding from portal colopathy)
Physical:
• Signs of portosystemic collateral formation include the following:
o Dilated veins in the anterior abdominal wall (umbilical epigastric vein
shunts)
o Venous pattern on the flanks (portal-parietal peritoneal shunting)
o Caput medusa (tortuous collaterals around the umbilicus)
o Rectal hemorrhoids
o Ascites - Shifting dullness and fluid wave (if significant amount of ascitic
fluid is present)
o Paraumbilical hernia
• Signs of liver disease include the following:
o Ascites
o Jaundice
o Spider angiomas

5. o Palmar erythema
o Asterixis
o Testicular atrophy
o Gynecomastia
o Dupuytren contracture
o Muscle wasting
o Splenomegaly
• Signs of hyperdynamic circulatory state include the following:
o Bounding pulses
o Warm, well-perfused extremities
o Arterial hypotension
Causes: Causes of increased resistance to flow are described as follows:
• Prehepatic
o Portal vein thrombosis
o Splenic vein thrombosis
o Congenital atresia or stenosis of portal vein
o Extrinsic compression (tumors)
o Splanchnic arteriovenous fistula
• Intrahepatic, predominantly presinusoidal
o Schistosomiasis (early stage)
o Primary biliary cirrhosis (early stage)
o Idiopathic portal hypertension (early stage)
o Nodular regenerative hyperplasia: Pathogenesis probably is obliterative
venopathy. The presence of nodules that press on the portal system also has
been postulated to play a role, although nodularity is present in most cases
without clinical evidence of portal hypertension.
o Myeloproliferative diseases: These act by direct infiltration by malignant
cells.
o Polycystic disease

6. o Hepatic metastasis
o Granulomatous diseases (sarcoidosis, tuberculosis): Clinical liver
dysfunction is rare in sarcoidosis. Portal hypertension is an unusual,
although well-recognized manifestation of hepatic sarcoidosis. Sarcoid
granulomas frequently localize in the portal areas, resulting in injury to the
portal veins.
• Intrahepatic, predominantly sinusoidal and/or postsinusoidal
o Hepatic cirrhosis
o Acute alcoholic hepatitis
o Schistosomiasis (advanced stage)
o Primary biliary cirrhosis (advanced stage)
o Idiopathic portal hypertension (advanced stage)
o Acute and fulminant hepatitis
o Congenital hepatic fibrosis
o Vitamin A toxicity: Noncirrhotic portal fibrosis is observed with various
toxic injuries, and one of these includes vitamin A toxicity. This probably is
due to vascular injury. Excessive doses of vitamin A taken for months or
years can lead to chronic hepatic disease. Intake of doses ranging from as
small as 3-fold the recommended daily dose continued for years to doses as
high as 20-fold the approved dose in a few months can lead to hepatic
disease. The pericellular fibrosis characteristic of vitamin A toxicity may
lead to portal hypertension.
o Peliosis hepatitis
o Venoocclusive disease
o Budd-Chiari syndrome
• Posthepatic
o Inferior vena cava (IVC) obstruction
o Right heart failure
o Constrictive pericarditis
o Tricuspid regurgitation
o Budd-Chiari syndrome
o Arterial-portal venous fistula
o Increased portal blood flow
o Increased splenic flow
Differential diagnosis:

7. Budd-Chiari Syndrome
Cirrhosis
Myeloproliferative Disease
Pericarditis, Constrictive
Polycystic Kidney Disease
Sarcoidosis
Schistosomiasis
Tricuspid Regurgitation
Tuberculosis
Vitamin A Toxicity
Work-up:
Lab Studies:
• Lab studies are directed towards investigating etiologies of cirrhosis, which is the
most common cause of portal hypertension. Lab studies include the following:
o Liver function tests
o Prothrombin time
o Albumin
o Viral hepatitis serologies
o Platelet count
o Antinuclear antibody, antimitochondrial antibody, antismooth muscle
antibody
o Iron indices
o Alpha1-antitrypsin deficiency
o Ceruloplasmin, 24-hour urinary copper - To be considered only in
individuals aged 3-40 years who have unexplained hepatic, neurologic, or
psychiatric disease
Imaging Studies:
• Duplex-Doppler ultrasonography
o Ultrasound (US) is a safe, economical, and effective method for screening
for portal hypertension. It also can demonstrate portal flow and helps in

8. diagnosing cavernous transformation of the portal vein, portal vein
thrombosis, or splenic vein thrombosis.
o Features suggestive of hepatic cirrhosis with portal hypertension include the
following:
 Nodular liver surface is suggestive. However, this finding is not
specific for cirrhosis and can be observed with congenital hepatic
fibrosis and nodular regenerative hyperplasia.
 Splenomegaly is a suggestive finding.
 Patients may demonstrate the presence of collateral circulation.
o Limitations of US include the following:
 Reproducibility of data is problematic.
 Many variables, such as circadian rhythm, meals, medications, and
the sympathetic nervous system, affect portal hemodynamics.
 Significant interobserver and intraobserver variation exist in
quantitative ultrasonographic measurement.
• CT scan
o CT scan is a useful qualitative study in cases where sonographic
evaluations are inconclusive.
o CT scan is not affected by patients' body habitus or the presence of bowel
gas.
o With improvement of spiral CT scan and 3-dimensional angiographic
reconstructive techniques, portal vasculature may be visualized more
accurately.
o Findings suggestive of portal hypertension include the following:
 Collaterals arising from the portal system are suggestive of portal
hypertension.
 Dilatation of the IVC also is suggestive of portal hypertension.
o Limitations of CT scan include the following:
 It cannot demonstrate the venous and arterial flow profile.
 Intravenous contrast agents cannot be used in patients with renal
failure or contrast allergy.
• Magnetic resonance imaging
o MRI provides qualitative information similar to CT scan when Doppler
findings are inconclusive.
o MRI angiography detects the presence of portosystemic collaterals and
obstruction of portal vasculature.

9. o MRI also provides quantitative data on portal venous and azygos blood
flow.
• Liver-spleen scan
o This is described for historical interest only.
o Liver-spleen scan uses technetium sulfur colloid taken up by cells in the
reticuloendothelial system.
o A colloidal shift from the liver to the spleen or bone marrow is suggestive
of increased portal pressure.
o Limitations include the following:
 Portal hypertension cannot be ruled out in the absence of this shift.
 Liver-spleen scan images lack spatial resolution.
 It has been superseded by US and CT scan.
Other Tests:
• Selective angiography of the superior mesenteric artery or splenic artery with
venous return phase
Procedures:
• Hemodynamic measurement of portal pressure
o Direct portal measurements usually are not performed due to the invasive
nature, the risk of complications, and the interference of anesthetic agents
on portal hemodynamics. The most commonly used method is
measurement of the hepatic venous pressure gradient (HVPG), which is an
indirect measurement that closely approximates portal venous pressure.
o A fluid-filled balloon catheter is introduced into the femoral or internal
jugular vein and advanced under fluoroscopy into a branch of the hepatic
vein. Free hepatic venous pressure (FHVP) then is measured.
o The balloon is inflated until it is wedged inside the hepatic vein, occluding
it completely, thus equalizing the pressure throughout the static column of
blood. The occluded hepatic venous pressure (ie, wedged hepatic venous
pressure) minus the unoccluded, or free, portal venous pressure (ie, FHVP)
is the HVPG.
• Endoscopy
o Perform upper endoscopy, as appropriate, to screen for varices in every
patient with suggestive findings of portal hypertension. Additionally, all

10. patients with cirrhosis should be considered for the presence of varices at
the time of the initial diagnosis of cirrhosis. Gastroesophageal varices
confirm the diagnosis of portal hypertension; however, their absence does
not rule it out. At times, gastroesophageal varices are incidental findings in
patients undergoing upper endoscopy for other reasons (eg, dyspepsia
refractory to medications, dysphagia, weight loss). These patients should
undergo further investigations for etiologies of portal hypertension.
o Various indirect indices, such as platelet count, spleen size, albumin, and
Child-Pugh score, have been studied to help diagnose varices without
endoscopy. A recent case review study revealed some of these predictors as
unreliable. For the time being, endoscopy remains the criterion standard for
screening patients with cirrhosis for varices.
o In compensated patients without varices, repeat endoscopy at 2- to 3-year
intervals to evaluate for the development of varices.
o In compensated patients with small varices, repeat endoscopy at 1- to 2-
year intervals to evaluate the progression of varices.
Histologic Findings: On liver biopsy, histologic findings are varied and depend not
only on the cause of liver disease but also on the cause of portal hypertension. Zone 3
necrosis can be observed in portal hypertension secondary to congestive heart failure
and Budd-Chiari syndrome. In cases of normal liver parenchyma, investigate for
prehepatic causes of portal hypertension.
Treatment:
Medical Care: Treatment is directed at the cause of portal hypertension.
Gastroesophageal variceal hemorrhage is the most dramatic and lethal complication of
portal hypertension; therefore, most of the following discussion focuses on the treatment
of variceal hemorrhage. Medical care includes emergent treatment, primary prophylaxis,
and elective treatment.
• Emergent treatment
o Bleeding from esophageal varices
 This ceases spontaneously in as many as 40% of patients. Each
episode of variceal bleeding is associated with a 30% mortality rate
and occurs mostly in patients with severe liver disease and in those
with early rebleeding. Rebleeding occurs in 40% of patients within 6
weeks.
 Following resuscitation, treatment of acute variceal bleeding includes
control of bleeding (24 h without bleeding within the first 48 h after
starting therapy) and prevention of early recurrence.
o Initial resuscitation with replacement of blood volume loss

11.  Blood should be replaced at a modest target of HCT of 25-30%.
 Avoid intravascular volume and variceal overexpansion to prevent
rebleeding.
o Diagnosis of source of bleeding
o Prevention of complications (eg, hepatic encephalopathy, bronchial
aspiration, renal failure, systemic infections, SBP)
 All patients with cirrhosis and upper GI bleeding are at a high risk of
developing severe bacterial infections, which are associated with
early rebleeding.
 The use of prophylactic antibiotics has been demonstrated to
decrease the rate of bacterial infections and increase survival rates,
thus prophylactic antibiotic use (norfloxacin 400 mg PO bid for 7 d;
ciprofloxacin and other broad-spectrum antibiotics also could be
used) in the setting of acute bleeding is recommended (Rimola,
2000).
o Specific treatment of bleeding lesion
o Pharmacological therapy
 Somatostatin (not available in the United States) is an endogenous
hormone that decreases portal blood flow by splanchnic
vasoconstriction at pharmacological doses, without significant
systemic adverse effects.
 Octreotide is a synthetic analogue of somatostatin that usually is
administered at a constant infusion of 50 mcg/h. Octreotide has been
shown to be effective in reducing the complications of variceal
bleeding after emergency sclerotherapy or variceal ligation.
 Vasopressin is the most potent splanchnic vasoconstrictor. It reduces
blood flow to all splanchnic organs, decreasing portal venous inflow
and decreasing portal pressure. Use of vasopressin is limited by
adverse effects related to splanchnic vasoconstriction (eg, bowel
ischemia) and systemic vasoconstriction (eg, hypertension,
myocardial ischemia). Continuous infusion of 0.2-0.4 IU/min (not to
exceed 0.8 IU/min) is recommended.
 Vasopressin always should be accompanied by intravenous
nitroglycerin at a dose of 40 mcg/min (not to exceed 400 mcg/min) to
maintain systolic blood pressure greater than 90 mm Hg.
 Adding nitrates to vasopressin therapy significantly improves
efficacy, although adverse effects of combination therapy are higher
than those associated with terlipressin or somatostatin.
 Terlipressin (not available in the United States) is a synthetic
analogue of vasopressin that has longer biological activity and
significantly fewer adverse effects than vasopressin.
 A recent randomized controlled trial showed that octreotide only
transiently reduced portal pressure and flow, whereas the effects of
terlipressin were sustained, suggesting that terlipressin may have

12. more sustained hemodynamic effects in patients with bleeding
varices.
o Endoscopic therapy
 Endoscopic therapy has the advantage of allowing specific therapy at
the time of diagnosis.
 Efficacy in achieving hemostasis is higher than 80%, but its
effectiveness declines to 70% at day 5 due to very early rebleeding in
some patients.
 Failures of endoscopic treatments may be managed by a second
session of endoscopic treatment, but no more than 2 sessions should
be allowed before deciding to perform transjugular intrahepatic
portosystemic shunt (TIPS) or surgery.
 Endoscopic injection sclerotherapy involves injecting a sclerosant
solution into the bleeding varix, obliterating the lumen by
thrombosis, or into the overlying submucosa, producing
inflammation followed by fibrosis. Several different sclerosants are
available: 5% sodium morrhuate, 1% to 3% sodium tetradecyl
sulfate, and 5% ethanolamine oleate. The typical volume used per
injection is 1-2 mL of sclerosant, with the total volume ranging from
10-15 mL.
 Complications of endoscopic injection sclerotherapy, which are more
frequent in acute bleeding than in elective situations, are related to
the toxicity of the sclerosant and include transient fever, stricture,
dysphagia, perforation (rarely), chest pain, mediastinitis, ulceration,
and pleural effusion.
 Endoscopic injection sclerotherapy is very effective emergency
treatment for acute variceal bleeding (not optimal for patients
bleeding from gastric fundal varices).
 Endoscopic variceal ligation (EVL) is achieved by a banding device
attached to the tip of the endoscope. The varix is aspirated into the
banding chamber, and a trip wire dislodges a rubber band carried on
the banding chamber, ligating the entrapped varix. One to 3 bands are
applied to each varix, resulting in thrombosis. EVL is less prone to
complications than injection sclerotherapy. EVL has the same
limitations of availability, cost, and difficulty in treating gastric
varices as sclerotherapy.
 Overall current data demonstrate clear advantages for using variceal
ligation over injection sclerotherapy. Endoscopic ligation requires
fewer endoscopic treatment sessions and causes substantially less
esophageal complications than injection sclerotherapy. However,
there is no overall survival benefit of variceal ligation over injection
sclerotherapy.
 Although ligation is being considered the treatment of choice for
esophageal varices, the choice of technique should be left up to the

13. experience of the operator, as well as the particular circumstances
found during endoscopic therapy.
o Other interventions
 Balloon-tube tamponade should be used only in massive bleeding as
a temporizing measure until definitive treatment can be instituted. An
endotracheal tube should be placed to protect the airway before
attempting to place the balloon tube. Complications are esophageal
and gastric ulceration, aspiration pneumonia, and esophageal
perforation. Continued bleeding during balloon tamponade indicates
an incorrectly positioned tube or bleeding from another source.
 The Minnesota tube has 4 lumens, 1 for gastric aspiration, 2 to inflate
the gastric and esophageal balloons, and 1 above the esophageal
balloon to suction secretions to prevent aspiration. The tube is
inserted through the mouth, and its position within the stomach is
checked by auscultation while injecting air through the gastric lumen.
The gastric balloon is inflated with 200 mL of air. Once fully
inflated, the gastric balloon is pulled up against the esophagogastric
junction, using approximately 0.5 kg of traction, compressing the
submucosal varices. The esophageal balloon rarely is required.
 The Minnesota tube is an adaptation of the Sengstaken-Blakemore
(S-B) tube, the difference is that the S-B tube does not have the
esophageal suction port to prevent aspiration.
 Endoscopic administration of cyanoacrylate monomer (superglue) in
gastric varices is another intervention.
• Primary prophylaxis: Primary prophylaxis is administered to patients at high risk
of bleeding. These patients have large varices, red wale markings on the varices,
and severe liver failure.
o Beta-blockers
 Beta-blockers include propranolol and nadolol. They are used most
commonly. Beta-blockers are noncardioselective and reduce portal
and collateral blood flow. Reduction in cardiac output (blockade of
beta1-adrenoreceptors) occurs. Splanchnic vasoconstriction
(blockade of vasodilatory adrenoreceptors of the splanchnic
circulation) also occurs.
 A recent meta-analysis of 11 trials evaluating nonselective beta-
blockers in the prevention of first variceal bleeding shows that the
bleeding rate in controls (25%) is significantly reduced (to 15%) in
patients treated with beta-blockers after a median follow-up of 24
months. The mortality rate also is lower in the beta-blocker group;
however, the difference does not achieve statistical significance. The
effect of beta-blockers as a function of variceal size also is analyzed.
The risk of first variceal bleeding in patients with medium-to-large
varices is 30% in controls, which is significantly reduced to 14% in

14. patients treated with beta-blockers. In patients with small varices, a
tendency exists for reduction in the first bleeding episode; however,
the number of patients and the rate of first bleeding are too low to
achieve statistical significance.
 Propranolol is administered at a dose of 20 mg every 12 h, which is
increased or decreased every 3-4 days until a 25% reduction in the
resting heart rate occurs or the heart rate is down to 55 beats per
minute (bpm). The average dose of propranolol usually is 40 mg bid.
Administering more than 320 mg/d is not recommended.
 Nadolol dosing is half the daily dose of propranolol, administered
once a day.
 Response to treatment is monitored by a reduction of the portal
pressure gradient by more than 20% of the baseline value or less than
12 mm Hg. Checking the HVPG response in primary prophylaxis is
not mandatory because 60% of patients who do not achieve these
targets do not bleed at 2-year follow-up evaluations.
 Propranolol is contraindicated in patients with asthma, chronic
obstructive pulmonary disease (COPD), atrioventricular (AV) block,
intermittent claudication, and psychosis. The most frequent adverse
effects are light-headedness, fatigue, dyspnea upon exertion,
bronchospasm, insomnia, impotence, and apathy. Reducing the dose
of propranolol frequently controls these adverse effects.
 Beta-blockers are best continued for the patient's lifetime because the
risk of variceal hemorrhage returns to that of the untreated population
once beta-blockers are withdrawn.
o Vasodilators
 Isosorbide mononitrate (ISMN) is a vasodilator and has been
demonstrated to reduce HVPG markedly in acute administration but
significantly less after long-term administration due to probable
development of patient tolerance.
 Vasodilators also reduce esophageal variceal pressure. The primary
concern in patients with advanced cirrhosis is that vasodilators can
reduce arterial blood pressure and promote the activation of
endogenous vasoactive systems that may lead to sodium and water
retention.
 One study reported ISMN to be as effective as propranolol in
preventing first variceal bleeding, but long-term follow-up of these
patients showed a higher mortality in patients older than 50 years in
the ISMN group.
 Available evidence does not support the use of ISMN as
monotherapy for primary prophylaxis, even in patients with
contraindications or intolerance to beta-blockers
o Combination therapy
 This involves both beta-blockers and ISMN. A large, double-blind,
placebo-controlled trial was unable to demonstrate a significantly

15. lower rate of first hemorrhage in the group treated with combination
therapy versus beta-blockers alone.
 Combination therapy appears to be associated with increased adverse
effects and a higher rate of ascites.
 Combination therapy cannot be recommended presently until further
studies prove efficacy.
o Prophylactic sclerotherapy
 Randomized controlled trials on the use of sclerotherapy for primary
prophylaxis produced divergent results, with some studies showing
worse outcome than controls.
 It has no role in primary prophylaxis.
o Prophylactic endoscopic variceal ligation
 EVL has been demonstrated to be more effective than no treatment in
preventing the first variceal bleed.
 Prophylactic EVL has been demonstrated to have an efficacy similar
to beta-blockers in prevention of first variceal bleed, but with
increased adverse effects.
 Prophylactic EVL currently cannot be recommended as a routine
measure for primary prevention but may be an option for patients
with grade 3 varices who have contraindications to or cannot tolerate
beta-blockers.
• Elective treatment: This is for the prevention of rebleeding. Variceal hemorrhage
has a 2-year recurrence rate of approximately 80%.
o Nonselective beta-blockers
 Propranolol and nadolol significantly reduce the risk of rebleeding
and are associated with prolongation of survival.
 Studies comparing propranolol with sclerotherapy in prevention of
variceal rebleeding demonstrate comparable rates of variceal
rebleeding and survival, but sclerotherapy was associated with
significantly more complications.
o Endoscopic sclerotherapy
 This usually is performed at weekly intervals.
 Approximately 4-5 sessions are required for eradication of varices,
which is achieved in nearly 70% of patients.
o Endoscopic variceal ligation
 EVL is associated with lower rebleeding rates and a lower frequency
of esophageal strictures. Fewer sessions are required to achieve
variceal obliteration when compared to sclerotherapy.
 EVL is considered the endoscopic treatment of choice in the
prevention of rebleeding. Sessions are repeated at 7- to 14-day
intervals until variceal obliteration (usually 2-4 sessions).
o Combination of EVL and pharmacologic therapy

16.  A recent randomized trial demonstrates that EVL plus nadolol plus
sucralfate is more effective in preventing variceal rebleeding than
EVL alone.
 Combination of EVL with beta-blockers seems to be reasonable for
patients in whom pharmacological therapy has failed.
Surgical Care: Surgical care includes decompressive shunts, devascularization
procedures, and liver transplantation.
• Decompressive shunts: These include total portal systemic shunts, partial portal
systemic shunts, and other selective shunts.
o Total portal systemic shunts
 These include any shunt larger than 10 mm in diameter between the
portal vein (or one of its main tributaries) and the IVC (or one of its
tributaries).
 Eck fistula (classic end-to-side portacaval shunt described for
historical interest only) was performed by Eck in dogs in the late
19th century. The portal vein is divided close to the liver, the hepatic
end of the portal vein is ligated, and the splanchnic end is
anastomosed to the IVC. This controls variceal bleeding and
decompresses splanchnic hypertension but leaves high pressure in the
hepatic sinusoids, thus ascites is not relieved.
 For the side-to-side portacaval shunt, the portal vein and the
infrahepatic IVC are mobilized after dissection and anastomosed. All
portal flow is directed through the shunt, and the portal vein itself
acts as an outflow from the obstructed hepatic sinusoids. Excellent
control of bleeding and ascites is achieved in more than 90% of
patients. Encephalopathy (rate of 40-50%) and progressive liver
failure are possible. The procedure has relatively limited indications,
which include massive variceal bleeding with ascites or acute Budd-
Chiari syndrome without evidence of liver failure.
o Partial portal systemic shunts
 These reduce the size of the anastomosis of a side-to-side shunt to 8
mm in diameter. Portal pressure is reduced to 12 mm Hg, and portal
flow is maintained in 80% of patients.
 The operative approach is similar to side-to-side portacaval shunts,
except the interposition graft must be placed between the portal vein
and the IVC.

17.  Two prospective, randomized, controlled trials revealed a 90% rate
for control of bleeding. Maintenance of some portal flow has
decreased the incidence of encephalopathy and liver failure.
o Selective shunts
 These provide selective decompression of gastroesophageal varices
to control bleeding while at the same time maintaining portal
hypertension to maintain portal flow to the liver.
 One example is the distal splenorenal shunt, which is the most
commonly used decompressive operation for refractory variceal
bleeding. It is used primarily in patients who present with refractory
bleeding and continue to have good liver function. It decompresses
the gastroesophageal varices through the short gastric veins, the
spleen, and the splenic vein to the left renal vein. Portal hypertension
is maintained in the splanchnic and portal venous system, and it
maintains portal flow to the liver. This shunt provides the best long-
term maintenance of some portal flow and liver function with a lower
incidence of encephalopathy (10-15%) compared to total shunts. The
operation produces ascites because the retroperitoneal lymphatics are
diverted.
• Devascularization procedures: These include splenectomy, gastroesophageal
devascularization, and esophageal transection (at times). Incidence of liver failure
and encephalopathy is low following devascularization procedures, presumably
because of better maintenance of portal flow. Devascularization could be used in
patients who are not candidates for decompression in whom first-line therapy has
failed. This includes patients who have portal or splenic vein thrombosis in
addition to cirrhosis.
o Splenectomy
 The spleen is one of the major inflow paths to gastroesophageal
varices. Splenectomy also allows better access to the gastric fundus
and the distal esophagus to complete the devascularization.
 Portal vein thrombosis of as much as 20% is reported following
splenectomy. Ascites is a frequent early postoperative complication
because portal hypertension is maintained.
o Gastroesophageal devascularization (Sugiura procedure)
 This should devascularize the whole greater curve of the stomach
from the pylorus to the esophagus and the upper two thirds of the
lesser curve of the stomach; the esophagus should be devascularized
for a minimum of 7 cm.
 In patients who have undergone extensive and repeated
sclerotherapy, the gastroesophageal junction is thickened and the
ability to perform a satisfactory transection is limited.
• Liver transplantation

18. o Liver transplantation is the ultimate shunt because it relieves portal
hypertension, prevents variceal rebleeding, and manages ascites and
encephalopathy by restoring liver function.
o It is the treatment modality that has significantly improved the outcome of
patients with Child-Pugh class C disease and variceal bleeding.
o Using liver transplantation in most patients is impractical because some
patients can be managed successfully with lesser methods; therefore,
transplant must be based on appropriate patient selections. For patients with
Child class A disease, shunt surgery is recommended; for patients with
Child class B disease, shunt surgery or TIPS is appropriate; and for people
with Child C class disease, TIPS or orthotopic liver transplant is
recommended.
• Primary prophylaxis: Surgery has no role for primary prophylaxis.
• Acute variceal bleeding
o The role of surgery in acute variceal bleeding is exceedingly limited
because therapy with endoscopic treatment controls bleeding in 90% of
patients.
o TIPS is a viable option and is less invasive for those whose bleeding is not
controlled. However, if TIPS is not available, then staple transection of the
esophagus is an option when endoscopic treatment and pharmacological
therapy have failed.
• Prevention of rebleeding
o For prevention of rebleeding, when pharmacological therapy and/or
endoscopic therapy have failed, consider surgery. Failure is defined as a
single episode of clinically significant rebleeding (transfusion requirement
of 2 U of blood or more within 24 h, a systolic blood pressure <100 mm Hg
or a postural change of >20 mm Hg, and/or pulse rate greater than 100
bpm) as per the Baveno II consensus conference on portal hypertension.
o TIPS is a useful procedure for continued bleeding despite medical and
endoscopic treatment in patients with Child class C disease and selected
patients with Child class B disease. It is effective only in portal
hypertension of hepatic origin.
 Technique: Under local anesthesia with sedation via the internal
jugular vein, the hepatic vein is cannulated and a tract is created
through the liver parenchyma from the hepatic to the portal vein with
a needle. This is performed under ultrasonographic and fluoroscopic
guidance. The tract is dilated, and an expandable metal stent is
introduced, connecting hepatic and portal systems. Blood from the
hypertensive portal vein and sinusoidal bed is shunted to the hepatic
vein.

19.  Indications: Accepted (established in controlled trials) indications
include (1) active variceal bleeding despite emergency endoscopic
and/or pharmacological treatment and (2) recurrent variceal bleeding
despite adequate endoscopic treatment. Potential (proven efficacy but
not adequately compared with that of existing therapies) indications
include (1) isolated bleeding from gastric fundic varices and (2)
refractory ascites. Experimental (efficacy not established in large-
scale trials) indications include (1) bleeding portal gastropathy, (2)
Budd-Chiari syndrome, (3) venoocclusive disease, (4) hepatorenal
syndrome, (5) hepatic hydrothorax, (6) bleeding ectopic varices, (7)
and protein-losing enteropathy due to portal hypertension.
 Causes of recurrent portal hypertension and bleeding after TIPS:
These include (1) continued esophageal bleeding; (2) stent
dysfunction (as many as 50% of shunts may occlude in 1 y) due to
stenosis, thrombosis, retraction, chinking, or displacement; (3)
hemobilia; and (4) persistent gastric varices associated with
spontaneous splenorenal collaterals or associated with massive
splenomegaly.
 Complications of TIPS related to technique: These include (1) neck
hematoma, (2) cardiac arrhythmia, (3) perihepatic hematoma, (4)
rupture of liver capsule, (5) extrahepatic puncture of portal vein, (6)
arterioportal fistula, and (7) portobiliary fistula.
 Complications of TIPS related to portosystemic shunting: These
include (1) hepatic encephalopathy (approximately 30%), (2)
increased susceptibility to bacteremia, and (3) liver failure.
 Other complications: These may include (1) TIPS-associated
hemolysis (approximately 10%) and (2) infection of stent.