2014 04 Varices Gastricas y Ectopicas (1)

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vessels into the portal system and simultaneous remodeling of the paired right and leftcardinal veins into the renal/adrenal/gonadal veins (subcardinal) and the azygous/ hemiazygos veins (supracardinal) lead ultimately to the mature venous system. Thedevelopment of these systems is important when approaching gastric varices (GV)

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and ectopic varices (ECV) because the connections that arise are often related to theiranatomic origins. For example, in patients with splenic vein thrombosis (SVT) and sub-sequent GV, the hypertensive short gastric veins in the fundus of the stomach, whichoriginate from the vitelline veins, often communicate with the azygous vein, which orig-inates from the s upracardinal veins, through small portosystemic collaterals in thedistal esophagus. 1 Understanding these anastomoses and the direction of theseveins afferent and efferent flow based on their anatomy can help gu ide therapeuticinterventions, which the authors note in future sections of this review. 2

GV IN CIRRHOSIS

In patients with cirrhosis and no underlying splanchnic vein thrombosis, studies havefound the prevalence of GV to be 17% to 25% compared with a prevalence of esoph-ageal varices (EV) of 50% to 60%. 3,4 GV bleed less frequently than EV but tend to bemore severe. 4 Fundal varices tend to bleed more often than varices in the cardia orantrum. 4 The natural history of GV has rarely been reported; but in one study of 132patients, the bleeding risk was estimated at 16%, 36%, and 44% at 1 year, 3 years,and 5 years, respectively. The presence of a red spot, a varix greater than 5 mm insize, and advanced Child-Pugh class were all found to be predictors of bleeding. 3

The absence of forward flow in the splenic vein has also recently been establishedas a predictor of GV bleeding, with a 5-year risk of 59% versus 39% when comparedwith those with forward flow. 5 This finding is consistent with a much earlier study thatnoted, in comparison with EV, GV are much more likely to have reversed or to-and-froflow in the splenic vein. 6

The management of GV in patients with cirrhosis depends greatly on how they areclassified because this can provide a guide for the prognosis and treatment approach.The most common system used is the Sarin classification ( Fig. 2 ).4 Using this classi-fication system helped identify gastric fundal varices as higher-risk lesions for bleedingand has guided other studies in evaluating responses to different therapies. Forinstance, sclerotherapy for GV has not had the same success that it had in the treat-ment of EV, except in subsets of patients with gastroesophageal varices (GOV) 1.Physiologically, this makes sense because, as the Sarin classification has shown,GOV1 GV are located near the gastroesophageal junction and are often fed fromthe same venous source as EV. However, with fundal varices, GOV2 and IGV 1, the

Sarin classification does not truly describe the underlying vascular heterogeneity,

Fig. 1. The embryologic development of the portal venous and systemic venous circulationof the abdomen. In gold are the vitelline veins that merge over time to form the intrahe-patic portal and hepatic veins as well as the superior portion of the intrahepatic inferiorvena cava (IVC). These veins also form the main portal vein and go on to form the splenicand mesenteric veins. In red are the umbilical veins. Over time, the right umbilical vein at-rophies and the left umbilical vein maintains a connection to the left portal venous systemand forms the ductus venosus with the vitelline veins; the ductus venosus becomes the lig-amentum venosum and the umbilical vein atrophies after birth. This vestigial link explainsthe presence of a recanalized umbilical vein in portal hypertension. Colored teal blue arethe paired subcardinal veins, which merge over time to form the abdominal IVC and bilat-eral renal, adrenal, and gonadal veins. In green are the azygous and hemiazygos veins,which are derived from the supracardinal veins and run inferiorly into the abdomen wherethe hemiazygos connects into the left adrenal vein. These vestigial connections should atro-phy over time but are likely the source of small portosystemic collaterals in portal hyperten-sion 1 and likely play a role in gastrorenal shunt formation. 2 SVC, superior vena cava.

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which has made it difficult to use this system alone to standardize an approach totreatment and highlights the need for a better understanding of the vascular anatomy.

Clinical investigators in the 1980s and 1990s, especially in Japan, can be creditedwith bringing a new appreciation of the architecture of the venous collateral bed un-derlying cardiofundal varices; these typically involve collaterals arising from the shortgastric veins and the posterior gastric veins leading to an outflow trunk that ends in theleft renal vein. 6 This study also highlights the difference between a right-sided portalcirculation and a left-sided portal circulation in relation to GV. Proposed vascular clas-sifications are based on the afferent veins feeding the varices combined with thevenous outflow tract, whether it is through a direct shunt or multiple small collaterals( Figs. 3 and 4 ).7,8 The vascular classifications can be used in conjunction with theendoscopic classification to determine the best therapy.

The management strategies for bleeding GV have varied over the years but aregenerally categorized into either endoscopic or radiologic approaches. Appropriate

Fig. 2. The Sarin endoscopic classification for GV. 4 GOV, gastroesophageal varices; IGV,

isolated GV.

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medical management of acute GV bleeding is unclear because there are no trials spe-cifically evaluating the use of octreotide or vasopressin analogues; however, the diver-sion of splanchnic blood flow should decrease bleeding similar to the effect seen inacute esophageal variceal bleeding and should be considered in this population.Balloon tamponade is likely a more effective method to stop bleeding in the acutesetting; however, this usually must be followed up by more definitive endoscopic orvascular therapy.

Fig. 3. The Kiyosue vascular classification of GV.7

Type 1 refers to a single afferent vein foreither the right or left portal circulation; type 2 refers to multiple afferent vessels contrib-uting to the varix; type 3 is consistent with type 2 with the addition of small afferent vesselsin direct continuity with the outflow track. Type A consists of a gastrorenal shunt (GRS) asthe sole outflow; type B describes the presence of a GRS in conjunction with small peri-diaphragmatic portosystemic collaterals; type C describes the presence of both a GRS anddirect gastro-caval shunt; type D consists of small portosystemic collaterals as the soleoutflow track. Types 1, 2, and 3 can be combined with types A, B, C, and D to describethe inflow and outflow of a GV.



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Endoscopic Treatment of GV

Endoscopic therapies have focused mainly on injection therapy with cyanoacrylateglues, but variceal band ligation has also been evaluated . Cyanoacrylate injectionhas excellent rates of acute hemostasis, greater than 90%, 914 but has variable rates

of rebleeding, with an average rate of around 20% within 1 year.9,10,13,15

Whencompared directly with band ligation, cyanoacrylate injection is superior at both initialhemostasis as well as long-term rebleeding. In one study, initial hemostasis was 87%with cyanoacrylate versus 45% with band ligation, with rebleeding rates of 31%versus 54%, respectively. 11 A more recent study comparing the two did not show adifference in acute hemostasis (both achieved 93%); however, rebleeding with cyano-acrylate was 23.0% at 1 year compared with 33.5% with the band ligation group. 9 Thisstudy also showed a much higher rate of recurrence of GV with band ligation versuscyanoacrylate, 60% versus 23%, respectively. One of the concerns with cyanoacry-late injection is the risk of embolization of the glue thrombus. The risk of severe and

potentially fatal embolization with the most commonly used 4-carbon N-butyl-2-cyanoacrylate is estimated to be 0% to 2%. 9,10,13,15 In one of the largest series, therisk of thrombotic complication was only 0.7%; these all occurred in a technique usinglarge volumes of lipiodol, which delays polymerization. 16 The authors own datacomparing the ex vivo polymerization times of various cyanoacrylate mixtures haveshown a roughly 2-fold increase in the polymerization time by adding the iodinatedplant oil ethiodized oil (Ethiodol) (identical to lipiodol) to N-butyl-2-cyanoacrylate.These results suggest that the use of iodinated contrast oils, although probablydecreasing the risk of needle impaction, increases the risk of embolization. 17

TIPS Treatment of GV

Transjugular intrahepatic portosystemic shunt (TIPS) has been evaluated in the treat-ment of GV. In comparison with EV, large GV often have lower portal pressures andlower portosystemic gradients before TIPS placement. 6,18 In a study from 1997, re-sults of TIPS procedures in patients with EV and/or GV were compared revealingthat EV had a notable reduction in size after TIPS, as would be expected; but 50%of GV did not change in size despite achieving a portosystemic gradient less than12 mm Hg. 19 These findings were again noted in a study from 2007 comparing cyano-acrylate injection with TIPS for the treatment of GV. Despite a slightly lower rebleeding

rate in the TIPS group when follow-up endoscopy was performed, those that under-went glue injection had a much lower r at e of persistent GV compared with the TIPSgroup, 20% versus 57%, respectively. 14 This phenomenon is likely caused by thepresence of spontaneous shunts, such as gastrorenal and splenorenal shunts. 6

In a study from 2003, TIPS had a lower 30-day rate of rebleeding when comparedwith cyanoacrylate injection, 15% versus 30%, respectively. But there was no mortal-ity difference between the groups, and the c ost analysis at 6 months revealed a sig-nificant benefit of glue injection over TIPS. 20 In the authors own data, they found alower 1-year rebleeding rate in the cyanoacrylate group compared with the TIPSgroup, 10% and 25% respectively, and also showed no mortality difference. 21 The au-thors did, however, show an increased morbidity with TIPS caused by hepatic en-cephalopathy. In an earlier study with this same population, the authors also founda cost benefit to cyanoacrylate treatment when compared with noncyanoacrylatetherapy. 22 Although TIPS remains a common and widely accepted means of manag-ing GV bleeding, its application remains problematic in many patients; it is sometimesineffective. 18,23 This ineffectiveness is especially so in patients with far-left shunts, inwhom transhepatic occlusion of the shunt, usually performed by delivering a coil



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endoscopic injection of cyanoacrylate along with one other patient with a red spot on aduodenal varix. All 3 acutely ble eding patients achieved initial hemostasis, and therewere no rebleeds among all 4. 46 Two other case reports reveal success with cyanoac-rylate injection with no rebleeding out to 1 yea r, an d another investigator reports suc-cess in a single case with thrombin injection. 4749 Most DV have an afferent venoussupply from either the portal vein or the superior mesenteric vein with an o utflow trackdirectly into the inferior vena cava, making TIPS and BRTO possible. 44,50 In one caseof failed endoscopic management, rescue BRTO was performed for DV bleeding withcomplete obliteration of the varix after 3 months of follow-up and no rebleeding. 51

Another series of 5 patients who underwent BRTO for DV reported 100% technicalsuccess and no rebleeding out to 1 year. 50 TIPS has also been successful in onecase report of DV in the setting of cirrhosis as a bridge to transplant. 52 Other reportson the general use of TIPS for all kinds of ECV bleeding have shown modest results inthe patients with DV. 53 Because of the lack of randomized trials, an exact recommen-dation for the treatment of DV cannot be made; but the evidence noted here suggeststhat, similar to GV, there are many viable modalities with similar rates of success.

COLORECTAL VARICES

Rectal varices (RV) are the most prevalent of the ECV, with rates reported as high as77% of all ECV. Their prevalence in patients with cirrhosis is between 28% and 56%,whereas their prevalence in extrahepatic portal vein obstruction is 63% to 94%. 5456

Bleeding from RV is rare but can be massive and fatal. 57,58 Most of the data on man-agement are related to TIPS placement in these patients; however, there are a fewcase reports and case series on endoscopic therapies, BRTO, and even surgical man-agement. Endoscopically there are case reports of cyanoacrylate use as well as bandligation. In contrast to GV, band ligation shows superior results with excellent initial he-mostasis and low rebleeding rates compared with glue injection. 5860 There have beencase reports of standard BRTO therapy as well as a transumbilical approach to aBRTO procedure; in both cases, the RV were completely obliterated and there wasno rebleeding. 61,62 There have been many retrospective studies evaluating TIPS re-sults in these patients; although initial hemostasis results are quite good, there arereble eding rates from 10% to 20% despite adequately reduced portal pres-sure. 53,6365 This finding is similar to the findings in some patients with GV afterTIPS and suggests that, because of the complex vascular outflow pathways seen inthese varices, TIPS alone may not be effective. In some cases, BRTO or TIPS withdirect embolization of the varix may be necessary.

GV AND ECV IN PORTAL VEIN THROMBOSIS

A discussion of GV and ECV would be incomplete without also addressing thesometimes-important role of portal vein thrombosis (PVT) whether in cirrhotic or non-cirrhotic patients.

Cirrhotic PVT and GV/ECV Bleeding

Cirrhotic patients with PVT and variceal bleeding have a much worse prognosis. 6669In addition, PVT is much more prevalent in cirrhotic patients when compared with thegeneral population, with an average prevalence around 10% and a range between2.1% and 23.0%. 70 There are only a few studies that remark on the incidence of PVT, one with a cumulative incidence of 7.4% and another with an annual incidenceof 16%. 71,72 The rates of variceal bleeding in cirrhotic patients with PVT range fromabout 39% to 50% at presentation; however, most of these bleeds are secondary



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to EV. 73 There are very little data regarding gastric variceal bleeding or ectopic varicealbleeding in cirrhotic patients with PVT; of the data available, there are only case re-ports or very small case series.

A case report of DV and GV in a patient with cirrhosis and PVT note d h emostasiswithout rebleeding out to 1 year after endoscopic injection of Histoacryl. 47 TIPS (usu-ally along with postprocedure anticoagulation) is also a viable option in these patient s,even with occlusive PVT provided intrahepatic portal branches can be visualized. 74

This approach has the advantage of offering variceal decompression but carries tech-nical challenges and an increased risk of hepatic decompensation with higher MELDscores. 19 There are a few prospective trials that have evaluated the use of anticoagu-lation in PVT related to cirrhosis and have noted very few bleeding events. 71,74,75 Inone of these studies, there was a significantly higher rate of recanalization in patientson anticoagulation; variceal bleeding was worse in patients that did not receive anti-coagulation compared with those that did. 74 Certainly, long-term anticoagulationneeds to be considered in this population, especially in patients with an underlyingthrombophilia.

Noncirrhotic PVT and GV/ECV Bleeding

Although cirrhosis-related portal hypertension may be the most common cause of GVand ECV, PVT and SVT are also known to cause both GV and ECV. Noncirrhotic PVT isthe second leading cause of portal hypertension in the Western world, with a preva-lence of 5% to 10% in patients with portal hypertension. 76 Within this group of pa-tients, EV are most prevalent at about 78% to 90% in all cases of noncirrhotic PVT,with GV having a reported prevalence from 14% to 50%. 68,7779 ECV have been re-

ported in 27% to 40% of cases of splanchnic vein thrombosis (PVT alone or withSVT or mesenteric vein thrombosis) and have been noted to be much more commonthan in cirrhosis. 55,77

In a study examining 60 patients with splanchnic vein thrombosis, 54 of which hadchronic noncirrhotic portal-mesenteric vein thrombosis, Orr and colleagues 78 notedthat 91% had EV on initial endoscopy and 50% had GV. Of those 60 patients, 50%presented with gastrointestinal bleeding. Of all bleeding events, the sentinel bleedingepisodes were from EV alone; but the secondary bleeding episodes were morecommonly GV and ECV, with bleeding rates of 26% and 33%, respectively. Fatal hem-orrhage was more often from GV and ECV, suggesting that, although less prevalent,

GV and ECV bleeding is more severe. A second study, by Spaander and colleagues, 80revealed similar results. They found that gastric fundal varices were associated with anincreased risk of rebleeding by a factor of 5 (hazard ratio 5.07). Despite rebleedingrisks, the overall mortal ity f or these patients is still more closely related to the under-lying cause of the PVT. 69,81

Anticoagulation in the setting of PVT remains a challenging aspect of treatment. Hy-percoagulable risks and myeloproliferative disorders (MPD) should be assessed. Theprevalence of an inherent clotting disorder, such as factor V Leiden, prothrombin mu-tation, protein C or S deficiency, or MPD, in these patients is 50% to 60% and can alterlong-term management in regard to anticoagulation. 68,8285 Currently, the Baveno Vcriteria, and other studies, recommend treating acute PVT for at least 3 to 6 months;however, if there is an underlying coagulopathy or MPD, then lifelong therapy needs tobe considered. 86,87 In contrast, the data for anticoagulation in chronic PVT, with cav-ernoma formation, are less persuasive but still suggest that, in the setting of a hyper-coagulable state, lifelong anticoagulation should be considered. The risk of bleedingwhile on anticoagulation is low, and some series showed that bleeding is less commonwith anticoagulation than without, likely because of decreased portal pressures

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secondary to recanalization. 78,88 Amitrano and colleagues 68 evaluated 121 patientswith PVT or mesenteric vein thrombosis noting all follow-up bleeding events occurredin the patients that were not on anticoagulation. Despite this low risk of bleeding fromvarices in this population, experts recommend screening for varices early after diag-nosis, performing follow-up endoscopy 6 months later, a nd t hen annually from thereon, treating the varices as you would in cirrhotic patients. 86,89 Although recanalizationdecreases the risk of bleedi ng, not all patients achieve recanalization. In separatestudies by Hall and Condat, 88,90 there were recanalization rates of 82% and 90%,respectively. 88,90 However, in most studies, the rates of recanalization on anticoagu-lation are in the range of 30% to 50%. 87,91 The rates of spontaneous recanalizationwithout anticoagulation range from 0% to 32% in these studies. 8690 Overall, the mor-tality risk in these patients is related to the thrombosis itself and/or the underlying dis-order causing the thrombosis and not from bleeding risk, suggesting thatanticoagulation is beneficial and should be considered in all patients, especially thosewith an underlying thrombophilic disorder. 69,92

Noncirrhotic SVT and GV/ECV Bleeding

SVT must also be considered separate from PVT and cirrhosis because the underlyingcause is much different. The most common causes of isolated SVT are chronicpancreatitis, acute pancreatitis, pancreatic pseudocyst, and neoplasm, with pancre-atitis the most frequent cause. 1,9397 The overall incidence of SVT ranges from 13%to 45%, with most of these studies evaluating populations of patients wi th panc rea-titis. It is estimated that 60% of cases of SVT are caused by pancreatitis. 94,9799 Theincidence of GV in SVT ranges from 15% to almost 57%, with higher rates in studies

that looked specifically at acute and chronic pancreatitis.1,93,94,98,99

The presentin gsymptom in patients w ith SVT is gastrointestinal bleeding in 45% to 72% of cases. 97

Heider and colleagues 93 looked at a large group of patients with pancreatitis over a10-year period and noted 53 that had SVT. Of these 53 patients, they initially reportedthat 41 of them were noted to have GV, a prevalence of almost 80%; however, most of these were noted on computed tomography findings. On further analysis, only 36 of these 53 patients underwent esophagogastroduodenoscopy (EGD); of those patients,only 11 had endoscopically notable GV, or about 30%. Another study by Agarwal andcolleagues 98 evaluated the incidence and management of SVT in patients with chronicpancreatitis. There was an incidence of SVT of 22% and, within that group, an inci-

dence of all varices of 41%. Of those with GV, 43% experienced a bleeding event.The definitive treatment of GV bleeding in the setting of SVT is splenectomy; however,

performing splenectomy in all patients with SVT is a contentious subject. 93,96,98 Heiderand colleagues 93 found that, in their patients with SVT, the overall bleeding risk was only4%; however, the patients that bled were all patients with GV on EGD. Additionally, Agarwal and colleagues 98 noted a bleeding rate from varices (EV vs GV not specified)of approximately 10% and also noted that, in patients who underwent splenectomy,there was no GV bleeding out to 2 years compared with a 14% GV bleeding rate in thosewho did not. This finding suggests that splenectomy may prevent GV bleeding.

SUMMARY

In conclusion, GV and ECV have several underlying causes and, therefore, cannot betreated with any one particular intervention. Acute management of both GV and ECVshould focus on the stabilization of patients while concurrently attempting to definethe underlying cause so that therapy can be tailored to the individual. More random-ized controlled trials are needed in the future to better define the subsets of



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