HEGAZY SURGERY

1. PORTAL HYPERTENSION
‫د‬.‫حجازى‬ ‫مصطفى‬

2. Practice Essentials
 The most common cause of portal
hypertension is cirrhosis.
 Vascular resistance and blood flow are 2
important factors in its development.

3. Signs and symptoms
 Weakness, tiredness, and malaise
 Anorexia, weight loss (common with acute
and chronic liver disease)
 Sudden and massive bleeding, with or without
shock on presentation
 Nausea and vomiting; abdominal discomfort
and pain
 Jaundice or dark urine

4. Signs and symptoms
 Edema and abdominal swelling (ascites);
splenomegaly
 Spider angiomas
 Males: Gynecomastia, testicular atrophy
(common with cirrhosis)
 Pruritus: Usually associated with cholestatic
conditions
 Spontaneous bleeding and easy bruising

5. Signs and symptoms
 Symptoms of encephalopathy: Sleep-wake
cycle disturbance; intellectual function
deterioration, memory loss, and an inability to
communicate effectively at any level;
personality changes; and, possibly, displays of
inappropriate or bizarre behavior
 Impotence and sexual dysfunction
 Muscle cramps (common in patients with
cirrhosis), muscle wasting

6. Signs and symptoms
 Dupuytren contracture
 Palmar erythema and leukonychia: May be
present in patients with cirrhosis
 Asterixis ("flapping tremor," "liver flap")

7. Complications of portal hypertension
 Hematemesis or melena: May indicate
gastroesophageal variceal bleeding or
bleeding from portal gastropathy
 Mental status changes: May indicate the
presence of portosystemic encephalopathy
 Increasing abdominal girth: May indicate
ascites formation

8. Complications of portal hypertension
 Abdominal pain and fever: May indicate
spontaneous bacterial peritonitis, although
this disease also presents without symptoms
 Hematochezia: May indicate bleeding from
portal colopathy

9. Signs of portosystemic collateral formation
 Anterior abdominal wall dilated veins: May
indicate umbilical epigastric vein shunts
 Venous pattern on the flanks: May indicate
portal-parietal peritoneal shunting
 Caput medusae (tortuous paraumbilical
collateral veins)

10. Signs of portosystemic collateral formation
 Rectal hemorrhoids
 Ascites
 Paraumbilical hernia

11. Signs of a hyperdynamic circulatory state
 Bounding pulses
 Warm, well-perfused extremities
 Arterial hypotension
 Flow murmur over the pericardium

12. Other signs of portal hypertension and
esophageal varices
 Pallor: May suggest active internal bleeding
 Parotid enlargement: May be related to
alcohol abuse and/or malnutrition
 Cyanosis of the tongue, lips, and peripheries:
Due to low oxygen saturation
 Dyspnea and tachypnea
 Telangiectasis of the skin, lips, and digits

13. Other signs of portal hypertension and
esophageal varices
 Fetor hepaticus: Occurs in portosystemic
encephalopathy of any cause (eg, cirrhosis)
 Small-sized liver
 Venous hums: Continuous noises audible in
patients with portal hypertension; may be
present as a result of rapid, turbulent flow in
collateral veins

14. Other signs of portal hypertension and
esophageal varices
 Tarry stool (digital rectal examination):
Suggests upper gastrointestinal (GI) bleeding
 Hemorrhoids

15. Diagnosis
Laboratory testing
 Complete blood count
 Liver function tests (eg, aspartate
aminotransferase [AST], alanine
aminotransferase [ALT], bilirubin, alkaline
phosphatase [ALP])
 Type and cross-match
 Coagulation studies (prothrombin time [PT],
partial thromboplastin time [PTT],
international normalized ratio [INR])

16. Diagnosis
Laboratory testing
 Blood urea nitrogen, creatinine, and
electrolytes
 Arterial blood gas (ABG) and pH
measurements
 Hepatic and viral hepatitis serologies,
particularly hepatitis B and C serologies

17. Other laboratory tests
 Albumin levels: Hypoalbuminemia is common
(impaired hepatic synthetic function)
 Antinuclear antibody, antimitochondrial
antibody, antismooth muscle antibody
 Iron indices

18. Other laboratory tests
 Alpha1-antitrypsin deficiency
 Ceruloplasmin, 24-hour urinary copper:
Consider this test only in individuals aged 3-40
years who have unexplained hepatic,
neurologic, or psychiatric disease

19. Imaging studies
 Duplex Doppler ultrasonography of the liver
and upper abdomen
 Computed tomography (CT) scanning and/or
magnetic resonance imaging (MRI): Can be
used when ultrasonographic findings are
inconclusive
 Bleeding scan or angiography: Used when
bleeding is obscure and the source is unclear

20. Procedures
 Liver biopsy and histologic examination
 Hemodynamic measurement of the hepatic
venous pressure gradient (HVPG): A criterion
standard for assessment of portal
hypertension
 Upper GI endoscopy (or,
esophagogastroduodenoscopy [EGD]): A
criterion standard for assessment of portal
hypertension

21. Management
 Treatment is directed at the cause of portal
hypertension.
 Gastroesophageal variceal hemorrhage is the
most dramatic and lethal complication of
portal hypertension; therefore, the focus is on
the treatment of variceal hemorrhage.
 Management of patients with liver cirrhosis
and ascites but without hemorrhage includes
a low-sodium diet and diuretics.

22. Emergent treatment
 Airway, breathing, and circulation evaluation
 Nasogastric tube placement with
hemodynamically significant upper GI
bleeding
 Nothing by mouth; establish 2 large-bore
venous accesses

23. Emergent treatment
 Volume resuscitation, with or without blood
product transfusion
 Portal pressure reduction (ie, anti-secretory
agent infusion)
 Patient transfer to tertiary center with liver
transplant service for uncontrolled bleeding
from portal hypertension
 Control and prevention of bleeding from
esophageal varices

24. Emergent treatment
 Prevention of complications (eg, prophylactic
antibiotics, combination
endoscopic/pharmacologic therapy)
 Administration of vasoconstrictors (eg,
octreotide [agent of choice in acute variceal
bleeding], vasopressin)
 Endoscopic therapy (variceal ligation [EVL]
[preferred], injection sclerotherapy)
 Balloon-tube tamponade

25. Emergent treatment
 Percutaneous transhepatic embolization (PTE)
 Endoscopic administration of cyanoacrylate
monomer
 Transjugular intrahepatic portosystemic shunt
(TIPS)

26. Primary prophylaxis
 Surveillance
 Nonselective beta-blockers (eg, propranolol,
nadolol)
 Vasodilators (eg, isosorbide mononitrate
[ISMN])
 Combination pharmacotherapy when a single
agent fails

27. Secondary prophylaxis
 Nonselective beta-blockers
 Endoscopic therapy (EVL, treatment of choice;
endoscopic sclerotherapy)
 Combination EVL and pharmacotherapy

28. Surgery
Surgery has no role in primary prophylaxis.
Consider procedures, such as the following,
for the prevention of rebleeding when
pharmacologic and/or endoscopic therapy
have failed:
 Portosystemic shunts
 Devascularization procedures
 Orthotopic liver transplantation: Treatment of
choice for advanced liver disease

29. Background
Many conditions are associated with portal hypertension,
with cirrhosis being the most common cause of this disorder.
Two important factors—vascular resistance and blood
flow—exist in the development of portal hypertension. 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, although in
most types of portal hypertension, both of these are altered.

30. Normal portal pressure is generally considered to be between
5 and 10 mm Hg.
Once the portal pressure rises to 12 mm Hg or greater,
complications can arise, such as varices and ascites.
Indeed, esophageal varices are responsible for the main
complication of portal hypertension, massive upper
gastrointestinal (GI) hemorrhage .

31. Pathogenesis
The portal vein carries approximately 1500 mL/min of
blood from the small and large bowel, the spleen, and the
stomach to the liver.
Obstruction of portal venous flow, whatever the etiology,
results in a rise in portal venous pressure.
The response to increased venous pressure is the
development of collateral circulation that diverts the
obstructed blood flow to the systemic veins.
These portosystemic collaterals form by the opening and
dilatation of preexisting vascular channels connecting the
portal venous system and the superior and inferior vena
cava.

32. Although high portal pressure is the main cause of the
development of portosystemic collaterals, other factors,
such as active angiogenesis, may also be involved.
The most important portosystemic anastomoses are the
gastroesophageal collaterals, which include esophageal
varices.
The gastroesophageal collaterals drain into the azygos vein.
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.

33. 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.

34. Portal vein and associated anatomy

35. Etiology and Pathophysiology
Increase in vascular resistance
 The initial factor in the etiology of portal
hypertension is the increase in vascular resistance to
the portal blood flow.
Poiseuille’s law, which can be applied to portal
vascular resistance, R, states that R = 8hL/pr4, where h
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. The lengths of the blood vessels in the
portal vasculature are relatively constant.

36. 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 = F8hL/pr4, where P is
portal pressure and F is portal blood flow).
Liver disease that decreases the portal vascular
radius produces a dramatic increase in portal vascular
resistance.
In cirrhosis, the increase occurs at the hepatic
microcirculation (sinusoidal portal hypertension).

37. Increased hepatic vascular resistance in cirrhosis is
not only a mechanical consequence of the hepatic
architectural disorder; a dynamic component also exists
due to the active contraction of myofibroblasts,
activated stellate cells, and vascular smooth-muscle
cells of the intrahepatic veins.
Endogenous factors and pharmacologic agents that
modify the dynamic component include those that
increase or decrease hepatic vascular resistance.

38. Factors that increase hepatic vascular resistance
include endothelin-1 (ET-1), alpha-adrenergic
stimulus, and angiotensin II.
Factors that decrease hepatic vascular resistance
include nitric oxide (NO),[6] prostacyclin, and
vasodilating drugs (eg, organic nitrates, adrenolytics,
calcium channel blockers).

39. Endothelin and nitric oxide
Studies have demonstrated the role of ET-1 and NO in the
pathogenesis of portal hypertension and esophageal varices.
ET-1 is a powerful vasoconstrictor synthesized by sinusoidal
endothelial cells that has been implicated in the increased hepatic
vascular resistance of cirrhosis and in the development of liver
fibrosis.
NO is a vasodilator substance that is also synthesized by
sinusoidal endothelial cells.
In the cirrhotic liver, the production of NO is decreased, and
endothelial nitric oxide synthase (eNOS) activity and nitrite
production by sinusoidal endothelial cells are reduced.
As a result, intrahepatic vasoconstriction occurs in cirrhotic liver
and accounts for approximately 20-30% of the increased
intrahepatic resistance.
Another major contribution to increased portal venous pressure is
the concomitant splanchnic arteriolar vasodilation causing
increased portal venous inflow.

40. Location of resistance in relation to the liver and sinusoids
Obstruction and increased resistance can occur at 3 levels in
relation to the hepatic sinusoids, as follows (see the Table,
below):
● Presinusoidal venous block (eg, portal vein thrombosis,
schistosomiasis, primary biliary cirrhosis) - Characterized by
elevated portal venous pressure and a normal wedged hepatic
venous pressure (WHVP); these abnormalities cannot be
detected by surrogate measurement (WHPV, HVPG), because
the measured pressure represents portal pressure in the
segment distal to the lesions, which is normal; however, direct
measurement of the portal venous pressure will be elevated

41. ● Postsinusoidal obstruction (eg, right sided heart failure, inferior
vena caval obstruction) - WHVP is characteristically elevated,
whereas the HVPG and FHVP can be either elevated or normal,
depending on the site of obstruction (intrahepatic postsinusoidal
vs posthepatic obstruction)
●Sinusoidal obstruction (eg, cirrhosis) - Characterized by HVPG,
FHVP, and WHVP, with WHVP being equal to portal venous
pressure (because disrupted intersinusoidal communications
diminishes compressibility and compliance of the sinusoids,
allowing direct transmission of portal pressure to the WHVP)

42. Etiology of Portal
Hypertension
WHVP FHVP HVPG
Prehepatic Normal Normal Normal
Intrahepatic Presinusoid
al
Normal Normal Normal
Sinusoidal Increased Increased Increased
Postsinusoi
dal
Increased Normal Increased
Posthepatic Budd-Chiari
syndrome
N/A Hepatic
vein cannot
be
cannulated
N/A
Other
posthepatic
causes
Increased Increased Normal
FHVP = free hepatic venous pressure; HVPG = hepatic venous
pressure gradient; N/A = not applicable; WHVP = wedged
hepatic venous pressure.
Table 1. Interpretation of Surrogate Portal Venous Pressure
Measurements in the Differential Diagnosis of Portal Hypertension

43. With regard to the liver itself, causes of
portal hypertension usually are
classified as prehepatic, intrahepatic,
and posthepat

44. Prehepatic resistance
Prehepatic causes of increased
resistance to flow include the
following:
•Portal vein thrombosis
•Splenic vein thrombosis
•Congenital atresia or stenosis of
portal vein
•Extrinsic compression (tumors)
•Splanchnic arteriovenous fistula

45. Intrahepatic resistance
Studies of hepatic microcirculation have
identified several mechanisms that may
explain increased intrahepatic vascular
resistance to flow. These mechanisms
may be summarized as follows :
•A reduction of sinusoidal caliber due to
hepatocyte enlargement
An alteration in the elastic properties of
the sinusoidal wall due to collagen
deposition in the space of Disse

46. • Compression of hepatic venules by
regeneration nodules
• Central vein lesions caused by perivenous
fibrosis
• Veno-occlusive changes
• Perisinusoidal block by portal
inflammation, portal fibrosis, and piecemeal
necrosis

47. More specifically, intrahepatic, predominantly
presinusoidal causes of resistance to flow
include the following:
• Schistosomiasis (early stage)
• Primary biliary cirrhosis (early stage)
• Idiopathic portal hypertension (early stage)
• Nodular regenerative hyperplasia - The
pathogenesis probably is obliterative
venopathy; the presence of nodules that press
on the portal system has also been postulated
to play a role, although nodularity is present in
most cases without clinical evidence of portal
hypertension

48. • Myeloproliferative diseases - These act via
direct infiltration by malignant cells
• Polycystic disease
• Hepatic metastasis
• Granulomatous diseases (sarcoidosis,
tuberculosis) - Clinical liver dysfunction is rare in
sarcoidosis, whereas 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

49. Intrahepatic, predominantly sinusoidal causes of
resistance include the following:
• Hepatic cirrhosis
• Acute alcoholic hepatitis
• Schistosomiasis (advanced stage)
• Primary biliary cirrhosis (advanced stage)
• Idiopathic portal hypertension (advanced stage)
• Acute and fulminant hepatitis
• Congenital hepatic fibrosis
• Peliosis hepatitis
• Veno-occlusive disease
• Budd-Chiari syndrome

50. • Vitamin A toxicity
• Sclerosing cholangitis
• Hepatitis B virus–related and hepatitis C virus–
related cirrhosis
• Wilson disease
• Hemochromatosis
• Alpha-1 antitrypsin deficiency
• Chronic active hepatitis

51. With regard to chronic active hepatitis, 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 for a few months can
lead to hepatic disease.
The pericellular fibrotic characteristic of vitamin A toxicity
may lead to portal hypertension.
Postsinusoidal obstruction syndrome and veno-occlusive
disease of the liver are postsinusoidal causes of
resistance

52. Posthepatic resistance
Posthepatic causes of resistance to flow
include the following:
• Thrombosis of the inferior vena cava (IVC)
• Right-sided heart failure
• Constrictive pericarditis
• Severe tricuspid regurgitation
• Budd-Chiari syndrome
• Arterial-portal venous fistula
• Increased portal blood flow
• Increased splenic flow

53. Increase in portal blood flow
The second factor that contributes to the pathogenesis
of portal hypertension is an increase in blood flow in the
portal veins.
This increase 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; the increased flow
contributes to the ability of portal hypertension to exist
despite the formation of an extensive network of
portosystemic collaterals that may divert as much as
80% of the portal blood flow.

54. 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.

55. Formation of varices
An elevated pressure difference between systemic and
portal circulation (ie, HVPG) directly contributes to the
development of varices.
HVPG is a surrogate marker of portal pressure gradient
and is derived from WHVP corrected (subtracted) with free
hepatic venous pressure (FHVP).
The hypertensive portal vein is decompressed by diverting
up to 90% of the portal flow through portasystemic
collaterals back to the heart, resulting in enlargement of
these vessels.
These vessels are commonly located at the
gastroesophageal junction, where they lie subjacent to the
mucosa and present as gastric and esophageal varices.

56. Varices form when the HVPG exceeds 10 mm
Hg; they usually do not bleed unless the HVPG
exceeds 12 mm Hg (normal HVPG: 1-5 mm Hg).
Gastroesophageal varices have 2 main inflows.
The first is the left gastric or coronary vein, and
the second is the splenic hilum, through the
short gastric veins.
The gastroesophageal varices are important
because of their propensity to bleed.

57. Normal venous flow through the portal
and systemic circulation. IMC = inferior
mesenteric vein; IVC = inferior vena cava;
SVC=superiorvenacav
Redirection of flow through the left
gastric vein secondary to portal
hypertension or portal venous
occlusion. Uphill varices develop in the
distal one third of the esophagus. IMC =
inferior mesenteric vein; IVC = inferior
vena cava; SVC = superior vena cava.

58. Mechanisms of variceal hemorrhage
Increased portal pressure contributes to
increased varix size and decreased varix wall
thickness, thus leading to increased variceal
wall tension. Rupture occurs when the wall
tension exceeds the elastic limits of the
variceal wall. Varices are most superficial at
the gastroesophageal junction and have the
thinnest wall in that region; thus, variceal
hemorrhage invariably occurs in that area

59. The following are risk factors for variceal hemorrhage:
Variceal size - The larger the varix, the higher the risk of rupture
and bleeding; however, patients may bleed from small varices too
The presence of endoscopic red color signs (eg, red wale
markings, cherry red spots)
Child B or C classification, especially the presence of ascites,
increases the risk of hemorrhage
Active alcohol intake in patients with chronic, alcohol-related liver
diseases
Local changes in the distal esophagus (eg, gastroesophageal
reflux) – These have been postulated to increase the risk of
variceal hemorrhage, but evidence to support this view is weak;
studies indicate that gastroesophageal reflux does not initiate or
play a role in esophageal hemorrhage.
Bacterial infection - A well-documented association exists
between variceal hemorrhage and bacterial infections, and this
may represent a causal relationship

60. Note that bacterial infection could also
trigger variceal bleeding through a
number of mechanisms, including the
following:
• The release of endotoxin into the
systemic circulation
• Worsening of hemostasis
• Vasoconstriction induced by the
contraction of stellate cells

61. Epidemiology
 Population-based prevalence data for portal
hypertension in the United States are not
available, but portal hypertension is a
frequent manifestation of liver cirrhosis.
 According to the National Institute on Alcohol
Abuse and Alcoholism (NIAAA), liver cirrhosis
accounted for almost 30,000 deaths in the
United States in 2007, making it the 12th
leading cause of US deaths.

62. Epidemiology
 The international incidence of portal
hypertension is also not known, although it is
probably similar to that of the US, with
differences primarily in the causes. In Western
countries, alcoholic and viral cirrhosis are the
leading causes of portal hypertension and
esophageal varices; 30% of patients with
compensated cirrhosis and 60-70% of patients
with decompensated cirrhosis have
gastroesophageal varices at the time of diagnosis.

63. Epidemiology
 The frequency of gastroesophageal varices
directly correlates with the severity of the
liver disease from 40% in Child class A to 85%
in Child class C.

64. Epidemiology
 The de novo rate of development of
esophageal varices in US patients with chronic
liver disease is approximately 8% per year for
the first 2 years and 30% by the sixth year. The
risk of bleeding from esophageal varices is
30% in the first year after identification.
 Bleeding from esophageal varices accounts for
approximately 10% of episodes of upper
gastrointestinal bleeding.

65. Epidemiology
 Hepatitis B is endemic in the Far East and
Southeast Asia, particularly, as well as in
South America, North Africa, Egypt, and other
countries in the Middle East.

66. Epidemiology
 Schistosomiasis is an important cause of
portal hypertension in Egypt, Sudan, southern
and sub-Saharan Africa, Southeast Asia,
Caribbean, and South America.
 Nonalcoholic steatohepatitis (NASH) is
becoming a major cause of liver cirrhosis in
the United States as hepatitis C is becoming a
major cause of liver cirrhosis worldwide.

67. Sex- and age-related demographics
 Liver disease demonstrates a sex predilection,
with males making up more than 60% of
patients with chronic liver disease and
cirrhosis.

68. Sex- and age-related demographics

69. Sex- and age-related demographics

70. Sex- and age-related demographics
 In general, alcoholic liver disease and viral
hepatitis are the most common causes for
esophageal varices in both sexes.

71. Sex- and age-related demographics
 However, veno-occlusive diseases and primary
biliary cirrhosis are more common in females;
and in females with esophageal varices,
alcoholic liver disease, viral hepatitis, veno-
occlusive disease, and primary biliary cirrhosis
are usually responsible.
 In males with esophageal varices, alcoholic
liver disease and viral hepatitis are usually the
cause.

72. Sex- and age-related demographics
 Portal vein thrombosis and secondary biliary
cirrhosis are the most common causes of
esophageal varices in children.
 Cirrhosis is the most common cause of
esophageal varices in adults.

73. Prognosis
 Patients with severe and persistent upper
gastrointestinal (GI) hemorrhage (ie, requiring
transfusions of >5 U of packed red blood cells)
have higher morbidity and mortality rate.

74. Prognosis
 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 estimated mortality rate for the first
episode of variceal hemorrhage is 30-50%.

75. Prognosis
 Patients with a known diagnosis of
esophageal varices have a 30% chance of
variceal bleeding within the first year after the
diagnosis.
 The mortality rate of the bleeding episode
depends on the severity of the underlying
liver disease.

76. Prognosis

77. Prognosis
 Patients who have had 1 episode of bleeding
from esophageal varices have a 60-80%
chance of rebleeding within 1 year after the
initial episode; approximately one third of
further bleeding episodes are fatal.

78. Prognosis
 The risk of death is maximal during the first
few days after the bleeding episode and
decreases slowly over the first 6 weeks.
 However, despite improvements in therapy,
the mortality rate at 6 weeks is remains
greater than 20%; this rate is higher when
surgical intervention is needed.

79. Prognosis
 Associated abnormalities in the renal,
pulmonary, cardiovascular, and immune
systems of patients with esophageal varices
contribute to 20-65% of deaths in these
individuals.
 Complications associated with portal
hypertension and GI bleeding include the
following:

80. Prognosis
 Hepatic encephalopathy
 Bronchial aspiration, aspiration pneumonia
 Renal failure
 Systemic infections, sepsis
 Spontaneous bacterial peritonitis
 Ascites
 Hepatorenal syndrome
 Bacteremia and/or endotoxemia

81. Prognosis
 Vascular collapse
 Cardiomyopathy
 Arrhythmias
 Hypotension
 Portal hypertensive gastropathy - This is a
common complication of cirrhosis and portal
hypertension, but significant bleeding from
this source is relatively uncommon

82. Prognosis
 Other complications include those related to
blood transfusion(s) and/or those related to
the therapeutic procedures used in the
management of bleeding varices.

83. Prognosis
Prognosis in patients with esophageal
varices
 Patients with a hepatic venous pressure
gradient (HVPG) of 20 mm Hg measured 24
hours after the onset of bleeding esophageal
varices have a higher 1-year mortality rate.

84. Prognosis
Prognosis in patients with esophageal
varices
 Other factors that can affect the prognosis of
patients with esophageal varices include the
following:
 Rebleeding

85. Prognosis
Prognosis in patients with esophageal
varices
 Child classification - Especially the presence of
ascites
 Active alcohol intake in patients with chronic,
alcohol-related liver diseases
 Occurrence of complications

86. Prognosis
 Several factors are known to influence the
prognosis of esophageal bleeding. These
include the following:
 The natural course of the disease causing
portal hypertension
 The severity of the portal hypertension
 The location and number of the bleeding
varices

87. Prognosis
 The functional status of the liver and the
severity of the liver disease - Early rebleeding,
within 5 days of admission; occurred in 21% of
patients classified as Child-Pugh grade A, 40%
of patients classified as grade B, and 63% of
patients classified as grade C
 Presence of associated systemic disorders
 Continued alcohol abuse
 Response to emergency treatment

88. Patient Education
 Educate patients about the benefits and
disadvantages of available treatment options.
 Alcohol intake should strongly be discouraged,
especially in patients with alcoholic cirrhosis.
Available resources for alcohol rehabilitation
should be provided, along with any
prophylaxis for alcohol withdrawal symptoms,
when indicated.

89. Patient Education
 Unless contraindicated, all patients with
esophageal varices should take beta-blockers
to reduce the risk of bleeding.
 Patients should also be educated about the
adverse effects of beta-blockers and the
possible risks of their abrupt discontinuation.

90. Patient Education
 Advise patients who have ascites of the risk of
spontaneous bacterial peritonitis during an
episode of acute variceal bleeding.