CHAPTER I INTRODUCTION Approximately 90% of patients with cirrhosis will have developed esophageal varices within 10 years.

Esophageal variceal haemorrhage is a devastating complication of cirrhosis with mortality as high as 2550%. ed sign and variceal si!e "medi#m to large grade$ on endoscopy are representative for %leeding ris& of esophageal varices. 'everity of liver f#nction reserve and presence of ascites are also important ris& factors for variceal %leeding. "1(2$ )he %leeding ris& decreases over time from the time that varices are identified* most %leeding episodes occ#r within the first 2 years after identification of varices. +nce %leeding occ#rs( spontaneo#s cessation of %leeding occ#rs in only #p to ,0% of individ#als( and the %leeding is associated with the mortality of 20% or more at - wee&s. ".(,$ /atients who s#rvived an episode of ac#te variceal hemorrhage have a high ris& of re%leeding and death. )he median re%leeding rate in #ntreated individ#als is aro#nd -0% within 102 years of the index %leeding( with a mortality of ..% . )herefore( care sho#ld %e ta&en to prevent rec#rrent %leeding prior to discharge from the hospital for patients who have recovered from an episode of variceal %leeding. "5(-$ )his paper will mainly disc#ss the esophageal varices as the complication of hepatic cirrhosis.

CHAPTER II
1

ANATOMY (7) )he liver is located in the right #pper 1#adrant( from the fifth intercostal space in the midclavic#lar line down to the right costal margin. )he liver weighs approximately 1200 g in men and 1,00 g in women. )he s#rfaces of the liver are smooth and convexin the s#perior( anterior( and right lateral regions. 3ndentations from the colon( right

&idney( d#oden#m ( and stomach are apparent on the posterior s#rface. )he line %etween the vena cava and gall%ladder divides the liver into right and left lo%es. Each lo%e has an independentvasc#lar and d#ct s#pply. )he liver is f#rther divided into eight segments( each containing a pedicle of portal vessels( d#cts( andhepatic veins. )he portal veno#s system extends from the intestinal capillaries to the hepatic sin#soid. )his veno#s system carries the %lood from the a%dominal gastrointestinal tract( the pancreas( gall%ladder( and spleen %ac& to the heart "co#rsing thro#gh the liver$. )he largest vessel in this system is the portal vein( which is formed %y the #nion of the splenic vein and s#perior mesentric veins. )he left gastric and right gastric veins and the posterior s#perior pancreaticod#odenal veins drain directly into the portal vein. )he portal vein r#ns posterior to the pancreas( and its extrahepatic length may %e anywhere from 59 cm. At the porta hepatis( it divides into the right and left portal veins within the liver( and the cystic vein typically drains into the right hepatic %ranch.

8ig 1. Anatomy of hepar and system portal

)he portal vein s#pplies 40% of the %lood flow to the liver( %#t only ,0% of the liver oxygen s#pply. )he remainder of the %lood comes from the hepatic artery( and %lood from %oth of these vessels mixes in the sin#soids. )he liver receives a tremendo#s vol#me of %lood( on the order of 1.5 liters per min#te. )he d#al %lood s#pply allows the liver to remain relatively resistant to hypoxemia. 5nli&e the systemic vasc#lat#re( the hepatic vasc#lar system is less infl#enced %y vasodilatation and vasoconstriction. )his is %eca#se the sin#soidal press#res remain relatively constant despite changes in %lood flow. A classic example is hepatic vein occl#sion res#lting in high sin#soidal press#re and extracell#lar extravasation of fl#id. )o maintain a constant inflow of %lood to the liver( hepatic artery %lood flow is inversely related to portal vein flow. )his appears to %e hormonally mediated rather than ne#rally mediated( since it persists in the transplanted liver.

CHAPTER III A. CIRRHOSIS HEPATIS

1. Definition 6irrhosis is a complication of many liver diseases that is characteri!ed %y a%normal str#ct#re and f#nction of the liver. )he diseases that lead to cirrhosis do so %eca#se they in7#re and &ill liver cells( and the inflammation and repair that is associated with the dying
3

liver cells ca#ses scar tiss#e to form. )he liver cells that do not die m#ltiply in an attempt to replace the cells that have died. )his res#lts in cl#sters of newly0formed liver cells "regenerative nod#les$ within the scar tiss#e.

2. Epidemio o!" 6hronic liver disease and cirrhosis res#lt in a%o#t .5(000 deaths each year in the 5nited 'tates. 6irrhosis is the ninth leading ca#se of death in the 5nited 'tates and is responsi%le for 1.2% of all 5' deaths. 9any patients die from the disease in their fifth or sixth decade of life. Each year( 2000 additional deaths are attri%#ted to f#lminant hepatic fail#re "8:8$. 8:8 may %e ca#sed viral hepatitis "eg( hepatitis A and ;$( dr#gs "eg( acetaminophen$( toxins "eg( Amanita phalloides, the yellow death0cap m#shroom$( a#toimm#ne hepatitis( <ilson disease( or a variety of less common etiologies. 6ryptogenic ca#ses are responsi%le for one third of f#lminant cases. /atients with the syndrome of 8:8 have a 50020% mortality rate #nless they are salvaged %y liver transplantation.

#. Etio o!" 3n western co#ntries the ca#ses of liver cirrhosis are common d#e to alcoholism( while in 3ndonesia( especially d#e to infection with hepatitis ; or 6 vir#s. )he res#lts in 3ndonesia said the most common ca#se of liver cirrhosis are hepatitis ; vir#s ".00,0%$( hepatitis 6 vir#s ".00,0%$( and #n&nown ca#ses "10020%$. As for some of the etiology of liver cirrhosis incl#de=

a$ Alcohol is a very common ca#se of cirrhosis( partic#larly in the <estern world. )he development of cirrhosis depends #pon the amo#nt and reg#larity of alcohol inta&e. 6hronic( high levels of alcohol cons#mption in7#re liver cells. %$ >onalcoholic fatty liver disease ">A8?@$ refers to a wide spectr#m of liver diseases that( li&e alcoholic liver disease( ranges from simple steatosis( to nonalcoholic steatohepatitis ">A':$( to cirrhosis. All stages of >A8?@ have in common the acc#m#lation of fat in liver cells. )he term nonalcoholic is #sed %eca#se >A8?@ occ#rs in individ#als who do not cons#me excessive amo#nts of alcohol( yet( in many respects( the microscopic pict#re of >A8?@ is similar to what can %e seen in liver disease that is d#e to excessive alcohol. >A8?@ is associated with a condition called ins#lin resistance( which( in t#rn( is associated with the meta%olic syndrome and dia%etes mellit#s type 2.+%esity is the most important ca#se of ins#lin resistance( meta%olic syndrome( and type 2 dia%etes. >A8?@ is the most common liver disease in the 5nited 'tates and is responsi%le for 2,% of all liver disease. 3n fact( the n#m%er of livers that are transplanted for >A8?@0related cirrhosis is on the rise. /#%lic health officials are worried that the c#rrent epidemic of o%esity will dramatically increase the development of >A8?@ and cirrhosis in the pop#lation. c$ 6ryptogenic cirrhosis "cirrhosis d#e to #nidentified ca#ses$ is a common reason for liver transplantation. 3t is termed cryptogenic cirrhosis %eca#se for many years doctors have %een #na%le to explain why a proportion of patients developed cirrhosis. @octors now %elieve that cryptogenic cirrhosis is d#e to >A': "nonalcoholic steatohepatitis$ ca#sed %y long standing o%esity( type 2 dia%etes( and ins#linresistance. )he fat in the liver of patients with >A': is %elieved to disappear with the onset of cirrhosis( and this has made it diffic#lt for doctors to ma&e the connection %etween >A': and cryptogenic cirrhosis for a long time. +ne important cl#e that >A': leads to
5

cryptogenic cirrhosis is the finding of a high occ#rrence of >A': in the new livers of patients #ndergoing liver transplant for cryptogenic cirrhosis. 8inally( a st#dy from 8rance s#ggests that patients with >A': have a similar ris& of developing cirrhosis as patients with long standing infection with hepatitis 6 vir#s. "'ee disc#ssion that follows.$ :owever( the progression to cirrhosis from >A': is tho#ght to %e slow and the diagnosis of cirrhosis typically is made in patients in their sixties. d$ 6hronic viral hepatitis is a condition where hepatitis ; or hepatitis 6vir#s infects the liver for years. 9ost patients with viral hepatitis will not develop chronic hepatitis and cirrhosis. 8or example( the ma7ority of patients infected with hepatitis A recover completely within wee&s( witho#t developing chronic infection. 3n contrast( some patients infected with hepatitis ; vir#s and most patients infected with hepatitis 6 vir#s develop chronic hepatitis( which( in t#rn( ca#ses progressive liver damage and leads to cirrhosis( and( sometimes( liver cancers. e$ 3nherited "genetic$ disorders res#lt in the acc#m#lation of toxic s#%stances in the liver which lead to tiss#e damage and cirrhosis. Examples incl#de the a%normal acc#m#lation of iron "hemochromatosis$ or copper "<ilsonAs disease$.

3n hemochromatosis( patients inherit a tendency to a%sor% an excessive amo#nt of iron from food. +ver time( iron acc#m#lation in different organs thro#gho#t the %ody ca#ses cirrhosis( arthritis( heart m#scle damage leading to heart fail#re( and testic#lar dysf#nction ca#sing loss of sex#al drive. )reatment is aimed at preventing damage to organs %y removing iron from the %ody thro#gh %loodletting "removing %lood$. 3n <ilson disease( there is an inherited a%normality in one of the proteins that controls copper in the %ody. +ver time( copper acc#m#lates in the liver( eyes( and %rain. 6irrhosis( tremor( psychiatric dist#r%ances and otherne#rological diffic#lties occ#r if

the condition is not treated early. )reatment is with oral medication that increases the amo#nt of copper that is eliminated from the %ody in the #rine. f$ /rimary %iliary cirrhosis "/;6$ is a liver disease ca#sed %y an a%normality of the imm#ne system that is fo#nd predominantly in women. )he a%normal imm#nity in /;6 ca#ses chronic inflammation and destr#ction of the small %ile d#cts within the liver. )he %ile d#cts are passages within the liver thro#gh which %ile travels to the intestine. ;ile is a fl#id prod#ced %y the liver that contains s#%stances re1#ired for digestion and a%sorption of fat in the intestine( as well as other compo#nds that are waste prod#cts( s#ch as the pigment %ilir#%in. ";ilir#%in is prod#ced %y the %rea&down of hemoglo%in from old red %lood cells.$. Along with the gall%ladder( the %ile d#cts ma&e #p the%iliary tract. 3n /;6( the destr#ction of the small %ile d#cts %loc&s the normal flow of %ile into the intestine. As the inflammation contin#es to destroy more of the %ile d#cts( it also spreads to destroy near%y liver cells. As the destr#ction of the hepatocytes proceeds( scar tiss#e "fi%rosis$ forms and spreads thro#gho#t the areas of destr#ction. )he com%ined effects of progressive inflammation( scarring( and the toxic effects of acc#m#lating waste prod#cts c#lminates in cirrhosis. g$ /rimary sclerosing cholangitis "/'6$ is an #ncommon disease fo#nd fre1#ently in patients with #lcerative colitis . 3n /'6( the large %ile d#cts o#tside of the liver %ecome inflamed( narrowed( and o%str#cted. +%str#ction to the flow of %ile leads to infections of the %ile d#cts and 7a#ndice and event#ally ca#ses cirrhosis. 3n some patients( in7#ry to the %ile d#cts "#s#ally as a res#lt of s#rgery$ also can ca#se o%str#ction and cirrhosis of the liver. h$ A#toimm#ne hepatitis is a liver disease ca#sed %y an a%normality of the imm#ne system that is fo#nd more commonly in women. )he a%normal imm#ne activity in
7

a#toimm#ne hepatitis ca#ses progressive inflammation and destr#ction of liver cells "hepatocytes$( leading #ltimately to cirrhosis. i$ 3nfants can %e %orn witho#t %ile d#cts "%iliary atresia$ and #ltimately develop cirrhosis. +ther infants are %orn lac&ing vital en!ymes for controlling s#gars that leads to the acc#m#lation of s#gars and cirrhosis. +n rare occasions( the a%sence of a specific en!yme can ca#se cirrhosis and scarring of the l#ng "alpha 1 antitrypsin deficiency$. 7$ ?ess common ca#ses of cirrhosis incl#de #n#s#al reactions to some dr#gs and prolonged expos#re to toxins( as well as chronic heart fail#re "cardiac cirrhosis$. 3n certain parts of the world "partic#larly >orthern Africa$( infection of the liver with a parasite "schistosomiasis$ is the most common ca#se of liver disease and cirrhosis.

$. P%t&o!ene'i'
8ig 2. 'tages of liver damage

?iver responds the cell damage %y forming extracell#lar matrix containing collagen( glycoproteins( and proteogli&ans. 'tellate cell extracell#lar matrix play a role in shaping this. 3n an ac#te in7#ry( stellate cells reshaping the extracell#lar matrix is th#s fo#nd to swelling of the liver. :owever( there are several factors that ca#se para&rine stellate cells into collagen0
8

prod#cing cells. /ara&rine factors may %e released %y hepatocytes( B#pffer cells( and sin#soidal endothelial response to prolonged in7#ry. 8or example( elevated levels of the cyto&ine transforming growth facto %eta 1 ")C80%eta1$ was fo#nd in patients with chronic hepatitis 6 and cirrhosis patients. )C80%eta1 then activates stellate cells to prod#ce collagen type 1 and #ltimately shrin&ing the si!e of the liver. 3ncreased deposition of collagen in the perisin#soidal and red#ced the si!e of hepatic endothelial fenestra ca#se &apilerisasi "s#ch as capillary endothelial pore si!e$ of the sin#soid. 'tellate cell in prod#cing the collagen to contract large eno#gh to s#ppress local presence perisin#soidal stellate cell contractility &apilarisasi and that ca#ses a lot of emphasis on the veins in the liver that disr#pts the %lood flow to the liver cells and liver cells event#ally die. :epatocyte death in large n#m%ers will ca#se a lot of damaged liver f#nction that ca#ses many clinical symptoms. /ress#re on the veins in the liver can lead to portal hypertension. /ortal hypertension is a ma7or ca#se of the state of the clinical manifestations.

(. Si!n %nd '"mtom'(12) 9any people with cirrhosis have no symptoms d#ring the early phases of the disease. 'ymptoms are ca#sed %y either of 2 pro%lems. Crad#al fail#re of the liver to carry o#t its nat#ral f#nctions and distortion of the liverAs #s#al shape and si!e %eca#se of scarring )he most common symptoms of cirrhosis are tiredness "fatig#e$ or even exha#stion( wea&ness( na#sea( loss of appetite leading to weight loss( loss of sex drive. 'ymptoms may not appear #ntil complications of cirrhosis set in. 9any people do not &now they have cirrhosis #ntil they have a complication. )he symtoms are fever( vomiting( diarhhea( 7a#ndice ( yellowing of the s&in and eyes from deposition of %ilir#%in in these tiss#es. ;ilir#%in is a prod#ct of the %rea&down of old %lood cells in the liver. 3tching can %e happen

from deposition in the s&in of prod#cts of the %rea&down of %ile. ;eside that( from fl#id retention ca#ses a%dominal swelling( edema( and diffic#lty %reathing. ;eca#se one of the f#nctions of the liver is secreting hormones( so in cirrhosis hepatic gynecomastia( scrotal swellin( and the a%normal menstr#al periods can %e fo#nd in this disease. ;leeding from g#ms or nose and easy %r#sing are often happend d#e to impaired prod#ction of clotting factors in cirrhosis.

CHAPTER III ). ESOPHA*EA+ ,ARICES

10

1. Definition Esophageal varices are a%normal( enlarged veins in the lower part of the esophag#s D the t#%e that connects the throat and stomach. Esophageal varices occ#r most often in people with serio#s liver diseases. Esophageal varices develop when normal %lood flow to yo#r liver is slowed. )he %lood then %ac&s #p into near%y smaller %lood vessels( s#ch as those in yo#r esophag#s( ca#sing the vessels to swell. 'ometimes( esophageal varices can r#pt#re( ca#sing life0 threatening %leeding.

2. Epidemio o!i Altho#gh varices can occ#r anywhere along the gastrointestinal tract t#%#lar( varices often occ#r in a few centimeters of the distal end of the esophag#s. Approximately 50% of patients with cirrhosis have gastroesophageal varices. Castric varices occ#r in 50..% of cases of portal hypertension. )he fre1#ency of esophageal varices ranged %etween .0040% in patients with cirrhosis( and 90.-% of patients with high0ris& varices. "11$

.. Etio o!" Esophageal varices are most often a complication of cirrhosis D irreversi%le scarring of the liver. +ther diseases and conditions also can ca#se esophageal varices. 6a#ses can incl#de= a$ 'evere liver scarring "cirrhosis$. A n#m%er of liver diseases can res#lt in cirrhosis( s#ch as hepatitis infection( alcoholic liver disease and a %ile d#ct disorder called primary %iliary cirrhosis. %$ ;lood clot "throm%osis$. A %lood clot in the portal vein or in a vein that feeds into the portal vein called the splenic vein can ca#se esophageal varices.
11

c$ A parasitic infection. 'chistosomiasis is a parasitic infection fo#nd in parts of Africa( 'o#th America( the 6ari%%ean( the 9iddle East and 'o#theast Asia. )he parasite can damage the liver( as well as the l#ngs( intestine and %ladder. d$ A syndrome that ca#ses %lood to %ac& #p in yo#r liver. ;#dd06hiari syndrome is a rare condition that ca#ses %lood clots that can %loc& the veins that carry %lood o#t of yo#r liver $. P%t&o!ene'i' 6irrhosis( the end stage of chronic liver disease( is the most common ca#se of portal hypertension. /ortal veno#s press#re "/$ is the prod#ct of vasc#lar resistance " $ and %lood flow "E$ in the portal %ed "+hmFs law* 8ig. 1$. 3n cirrhosis( %oth intrahepatic vasc#lar resistance and portal flow are increased. /ortal hypertension leads to the formation of portosystemic collaterals. :owever( d#e to their higher resistance and increased portal veno#s inflow( these collaterals are #na%le to decrease the hypertension. /ortal hypertension is %est assessed "indirectly$ #sing the wedged hepatic veno#s press#re "<:G/$ meas#rement. A press#re difference %etween the portal and systemic circ#lation "the hepatic veno#s press#re gradient( :G/C$ of 1012 mm:g is necessary "%#t not s#fficient$ for varices to form. )he normal :G/C is .5 mm:g. 'ingle meas#rements are #sef#l for determining the prognosis of %oth compensated and decompensated cirrhosis( while repeat meas#rements are #sef#l for monitoring the response to pharmacological therapy and the progression of liver disease."10$ Garices r#pt#re if the wall tension %ecomes too great. )he li&elihood that a varix will r#pt#re and %leed increases with increasing si!eHdiameter of the varix and with increasing variceal press#re( which is again proportionate to the :G/C. 6onversely( varices do not %leed if the :G/C is %elow 12 mm:g. )he ris& of re%leeding decreases significantly with red#ctions in :G/C greater than 20% from %aseline. "11$
12

(. Si!n %nd '"mtom' Esophageal varices #s#ally donAt ca#se signs and symptoms #nless they %leed. 'igns and symptoms of %leeding esophageal varices incl#de= 'hoc&( in severe cases Gomiting %lood ;lac&( tarry or %loody stools

-. Ri'. f%/to0 An international normali!ed ratio "3> $ score I 1.5( a portal vein diameter of I 1. mm( and throm%ocytopenia have %een fo#nd to %e predictive of the li&elihood of varices %eing present in cirrhotics. 3f none( one( two( or all three of these conditions are met( then J 10%( 2050%( ,0-0%( and I 90% of the patients are estimated to have varices( respectively. )he presence of one or more of these conditions represents an indication for endoscopy to search for varices and carry o#t primary prophylaxis against %leeding in cirrhotic patients. "10(11$

CHAPTER I, DISCUSSION

Esophageal varices are the ma7or complication of portal hypertension. 3t is detected in a%o#t 50% of cirrhosis patients( and approximately 515% of cirrhosis patients show newly formed varices or worsening of varices each year.

13

As other parenchyma tiss#e( the liver normally contains epithelial component "hepatocytes$( endothelial layer "of the liver characteri!ed %y the presence fenestra$( tiss#e macrophages "B#pffer cells$( and perivasc#lar mesenchymal cells called stelata cells. 'telata cells that are normally involved in the storage of fat and vitamin A will %e transformed into cells that resem%le miofi%ro%las in case of in7#ry in the liver. )his led a change in the extracell#lar matrix( the prod#ction of collagen %ecome increase and forming tiss#e fi%rosis. 6ontraction of activated stellate cells is promoted %y increased vasoconstrictor endothelin and a red#ction in the vasodilator nitric oxide within the liver. )herefore( intrahepatic resistance increases. 3n contrast to its intrahepatic levels( nitric oxide concentrations are elevated in the peripheral and splanchnic circ#lation. )his res#lts in decreased systemic and splanchnic vasc#lar resistance( th#s increasing portal %lood flow."1,$

6irrhosis
3ncreased splanchnic K peripheral >+ @ecreased intrahepatic >+

@ecreased systemic K splanchnic vasc#lar resistance

3ncreased intrahepatic resistance

6ollaterals
3ncrease portal %lood flow 9aintains portal hypertension 'odi#m retention

14

8ig .. )he pathogenesis of oesophageal varices

/ortal hypertension is associated with %oth increased portal inflow and increased o#tflow resistance. )he portal hypertension is directly related to portal inflow andHor o#tflow resistance(as determined %y +hmFs law Lportal press#re M portal veno#s inflow o#tflow resistance.N /ortal veno#s inflow is affected %y hyperdynamic circ#lation( which is characteri!ed %y systemic and splanchnic vasodilatation( low systemic resistance( plasma vol#me expansion( and high cardiac index. 'planchnic vasodilatation contri%#tes to increasing s#%stantial %lood vol#me which ret#rns to portal veno#s system. /eripheral vasodilatation activates endogeno#s ne#roh#moral systems that ca#se sodi#m retention( which leads to expansion of the plasma vol#me( followed %y an increase in the cardiac index."1.$ +ne of the potential for comm#nication %etween circ#lation splancnic intraa%dominal and systemic veno#s circ#lation is thro#gh the esophag#s. 3f the portal veno#s %lood flow to the liver is hampered %y cirrhosis or other ca#ses( portal hypertension that occ#r trigger the formation of collateral %ypass channels in a meeting place for portal and systemic systems. )herefore( the portal %lood flow diverted thro#gh the stomach into the coronary veno#s plex#s of s#%epithelial and s#%m#cosal esophageal veins( then into the a!ygos vein and s#perior vena cava. 3ncreased press#re in the esophageal plex#s ca#ses them to dilate and winding serpentine &nown as varices. /atients with cirrhosis are experiencing varices at a rate

15

of 5% 015% per year( so that the veins fo#nd in approximately two0thirds of all patients with cirrhosis. "1.$

8ig ,. Esophageal varices

#pt#red varices occ#r when the strain in the wall of varices is too %ig. /ossi%le wall varices "varix$ will have a tear in line with the magnit#de H diameter varix variseal and with increased press#re( which again is e1#ivalent to the :G/C. <all varices will not tear if :G/C press#re less than 12 mm:g. 3n ideal circ#mstances( patients with &nown varices sho#ld receive treatment to red#ce their ris& of %leeding. )he non0selective O0

%loc&ers "e.g.( propranolol 10 mg ( timolol or nadolol20 mg$ and nitrates "e.g. isosor%ide mononitrate "39>$ 20 mg ;@$ have %een eval#ated for primary prophylaxis. >on0 selective O0%loc&ers "%#t not cardioselective O0%loc&ers li&e atenolol$ are preferred %eca#se they decrease %oth cardiac o#tp#t %y O1 %loc&ade and splanchnic %lood flow %y %loc&ing

16

vasodilating O2 receptors at splanchnic vasc#lat#re. )he effectiveness of this treatment has %een shown %y a n#m%er of different st#dies."15(1-$ Endoscopic variceal %and ligation may %e an alternative for patients who cannot tolerate( or have contraindications to %eta0%loc&ers. )he %est approach for patients with ac#te variceal %leeding is the com%ination of vasoactive dr#gs and endoscopic therapy. )erlipressin is administered as 2mg 3G %ol#s and 1mg every six ho#rs for 205 days. 'omatostatin is given as an 3G 250mcg %ol#s followed %y 250mcgHho#r inf#sion and octreotide is administered as a %ol#s in7ection of 50mcg followed %y an inf#sion at a rate of 50mcgHho#r. 'omatostatin or octreotide therapy sho#ld %e maintained for 5 days to prevent early re0%leeding. egarding

endoscopic therapy( EG? is preferred %#t sclerotherapy may %e #sed depending on the endoscopistFs experience and the partic#lar circ#mstances fo#nd d#ring endoscopy. "14(12$ )he first0line treatment for prevention of rec#rrent variceal haemorrhage is %eta%loc&ers( endoscopic variceal ligation or the com%ination of %eta0%loc&ers and endoscopic variceal ligation. )3/' or s#rgical sh#nt appears to %e more appropriate for patients who are non0compliant or refractory to pharmacological and endoscopic therapy."19$

?arge varices "Crade .$ or moderate varices "Crade 2$ with endoscopic red wale signs or 6hildFs 6 cirrhosis

A+*ORITHM1 PRIMARY PROPHY+A2IS O3 ,ARICEA+ )+EED

;eta0%loc&er therapy "propranolol 10 mg ( timolol or nadolol20 mg$ and nitrates "e.g. isosor%ide mononitrate "39>$ 20 mg ;@$$ 17 3f 6hildFs 6 cirrhosis consider liver transplant

EG? if %eta0%loc&er contraindicated or intolerant

'#spected ac#te variceal %leeding "AG;$

es#scitation( 3G access( CP9

)erlipressin H +ctreotide H 'omatostatin for 205 days Anti%iotic /rophylaxis for 4 days in patients with cirrhosis Endoscopy service #navaila%le ;alloon tamponade if active %leeding )ransfer to endoscopy centre 5rgent Endoscopy

+esophageal varices

Castric varices

A+*ORITHM1 MANA*EMENT O3 ACUTE ,ARICEA+ )+EEDIN*cyanoacrylate sclerotherapy if EG?

diffic#lt

EG? preferred*

3n7ection with

/ersistent active %leeding

/ersistent active %leeding

>+

QE'

)3/' or s#rgical intervention

;eta0%loc&ers( EG? or %oth

18

epeat endoscopic therapy )3/' or s#rgical sh#nt

CHAPTER , CONC+USION 6irrhosis is a condition that is defined histopathologically and has a variety of clinical manifestations and complications( some of which can %e life0threatening( portal hypertension is directly responsi%le for the ma7or complications of cirrhosis( variceal hemorrhage. Gariceal hemorrhage is an immediate life0threatening pro%lem with a 20.0% mortality associated with each episode of %leeding.
19

3n normal condition( the liver has system receives %lood from the mesenteric veins( stomach( lymph nodes( and pancreas enter thro#gh the hepatic artery and portal vein. ;lood sent to the liver via the portal triad consisting of a %ranch of the portal vein( hepatic artery and %ile d#ct. )hen it will contino#s to the lo%#l liver sin#soid space. ;lood that has filtered into the central vein and then into the hepatic vein larger toward the inferior vena cava. 3n cirrhosis( the presence of fi%rotic tiss#e in the sin#soids interfere the normal %lood flow to the liver lo%#l( it will ca#se the portal hypertension that can develop into varices. )here are treatments to stop %leeding in s#ch as vaso0active dr#gs( vasopressin( somatostatin( octreotide( endoscopic sclerotherapy and %anding, and endoscopic variceal ligation. R0;loc&ers and endoscopic variceal %and ligation are the treatments to prevent %leeding.

RE3ERENCES 1. . @e 8ranchis and 9. /rimignani( L>at#ral history of portal hypertension in patients with cirrhosis(N Clinics in Liver Disease( vol. 5( no. .( pp. -,5--.( 2001. 2. 6. 9er&el( 9. Soli( '. 'iringo et al.( L/rognostic indicators of ris& for first variceal %leeding in cirrhosis= a m#lticenter st#dy in 411 patients to validate and improve the >orth 3talian Endoscopic 6l#% ">3E6$ index(N American Journal of Gastroenterology( vol. 95( no. 10( pp. 29152920( 2000.

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..

C. @FAmico and . @e 8ranchis( L5pper digestive %leeding in cirrhosis. /ost0therape#tic o#tcome and prognostic indicators(N Hepatology( vol. .2( no. .( pp. 599-12( 200..

,.

>. 6ar%onell( A. /a#wels( ?. 'erfaty( +. 8o#rdan( G. C. ?Tevy( and

. /o#pon(

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15. ?e%rec @( /oynard )( :illon /( ;enhamo# U0/ "1921$. [/ropranolol for prevention of rec#rrent gastrointestinal %leeding in patients with cirrhosis= a controlled st#dy[. # $ngl J !ed #4( "2.$= 1.411.4,. 1-. )alwal&ar UA( Bamath /' "200,$. [An evidence0%ased medicine approach to %eta0 %loc&er therapy in patients with cirrhosis[. Am J !ed11- "11$= 4594--. 14. Cros!mann U( Carcia0)sao C( ;osch U( et al" "2005$. [;eta0;loc&ers to /revent

Castroesophageal Garices in /atients with 6irrhosis[. # $ngl J !ed #(# "21$= 225, 22-1. 12. Barsan :A( 9orton '6( 'he&elle /C( et al. 6om%ination endoscopic %and ligation and sclerotherapy compared with endoscopic %and ligation alone for the secondary prophylaxis of esophageal variceal hemorrhage= a meta0analysis. Dig Dis Sci. 2005*50"2$=.990,0-. 19. osch U( Beller 8'. )rans7#g#lar intrahepatic portosystemic sh#nt= present stat#s( comparison with endoscopic therapy and sh#nt s#rgery( and f#t#re prospectives. %orld J Surg. 2001*25".$=..40,5.

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