Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3657_Библиотеки_им_академика_М_И_Перельмана.pdf
Скачиваний:
0
Добавлен:
30.08.2026
Размер:
49 Мб
Скачать
424
Fig. 38.4 Wedged venogram with reux of carbon dioxide into the
portal venous system (red arrow), which provides a guiding map for the creation of the TIPS. Inated balloon is visualized at the tip of the hepatic venous catheter (blue arrow)
R. Koppula and Z. J Haskal
• Budd-Chiari syndrome: Although TIPS is more technically challenging in these cases, it is recommended when conser­vative measures such as anticoagulation and thrombolysis fail and has been shown to improve transplant-free survival (78% at 5 years) [36]. For this indication, a higher PSG (15mmHg) is often sufcient as portal pressures rapidly decrease with auto-diuresis [37].
Patients are monitored overnight on the oor or in the
ICU, depending on their pre-procedure condition. It is important to track changes in mental status, urine output, liver function tests and serum creatinine. Progressively wors­ening pain may indicate acute post-procedural bleeding, which should be worked up by trending hemoglobin levels and CT imaging as necessary. Baseline TIPS Doppler ultra­sound should be performed no sooner than 72 h after the procedure, as PTFE grafts reect ultrasound waves in this initial period and can falsely resemble in-stent thrombosis. Excessive uid resuscitation should be avoided in the imme­diate post-procedure period to minimize the risk of pulmo­nary edema and heart failure caused by the increased right atrial pressures and cardiac preload seen after TIPS creation.
Fig. 38.5 (a) Placement of the TIPS needle (blue arrow) into the portal
vein (red arrow) conrmed by injection of contrast. (b) Splenic (green arrow) venography and pressure measurement demonstrated a portosys­temic gradient of 18mmHg. Note the opacication of esophageal vari­ces (red arrow) and the inferior mesenteric vein (blue arrow). (c) The parenchymal tract is dilated to 8mm. (d) Final splenic venogram after
TIPS placement demonstrates a decreased PSG (10mmHg), with loss of opacication of the varices and inferior mesenteric vein as seen in (b). An overlapping stent graft was placed to cover the remaining segment of bare hepatic vein (not shown). Note the transition between the bare (red) and covered (blue) portions of the stent
38 Transjugular Intrahepatic Portosystemic Shunt (TIPS) andPortal Hypertension
425
Table 38.3 Acute complications after TIPS
Major complications (3%) Minor complications (4%) Stent malposition (1%) Transient contrast-induced kidney
Hemobilia (2%) Fever (2%) Gallbladder injury (1%) Entry site hematoma (2%) Hemoperitoneum (0.5%) Radiation skin burn (0.1%) Liver infarction (0.5%) Encephalopathy (5-35%) Renal failure requiring dialysis (0.25%) Hepatic artery injury (1%) Death (1%)
injury (2%)
Transient pulmonary edema (1%)
Management includes uid restriction and diuresis as nec­essary. Acute complications associated with TIPS procedure are summarized in Table38.3 [38].
Patients should be seen in clinic 3–4weeks after the pro­cedure. A focused physical exam and liver function tests should be performed to monitor for side effects such as liver failure and hepatic encephalopathy. When ascites is the indi­cation, additional paracenteses may be required for several weeks after the TIPS.Follow-up clinic visits should be per­formed at 3, 6, and 12months during the rst year and at 6months intervals thereafter to assess for complications and symptoms of recurrent portal hypertension.
Worsening hepatic encephalopathy (HE) is seen in 5–35% of patients after TIPS, with increased incidence in patients receiving TIPS for refractory ascites, with poor baseline liver function, and patients with a prior history of HE [39]. Approximately 90% of cases present in the rst 3 months after TIPS creation. First-line therapy is oral lactulose with dose titration to 2–3 bowel movements a day. Oral rifaximin (500mg BID) is effective in reducing hepatic encephalopa­thy without signicant systemic side effects. A protein restricted diet and branch-chain amino acids are additional conservative therapies. Approximately 7% of patients expe­rience varying degrees of refractory encephalopathy [40]. The West Haven criteria is a semiquantitative method of grading and communicating the severity of symptoms seen in hepatic encephalopathy (Table 38.4) [41]. In cases of refractory HE, the TIPS can be downsized via placement of a smaller diameter stent within the original graft. Intentional thrombosis of the TIPS can be performed using coils or bal­loons, although these measures should be reserved for severe and debilitating encephalopathy due to the risk of recurrent variceal bleeding and decrease in renal blood ow.
Table 38.4 West Haven criteria for grading hepatic encephalopathy
Grade Description I Trivial lack of awareness
Euphoria or anxiety Shortened attention span Impaired performance of addition
II Lethargy or apathy
Minimal disorientation for time or place Subtle personality change, inappropriate behavior Asterixis, slurred speech Impaired performance of subtraction
III Somnolence to semi-stupor, hyperreexia/rigidity
Gross disorientation
IV Coma (unresponsive to verbal or noxious stimuli)
TIPS stenoses most often occur in segments of unstented hepatic vein adjacent to the TIPS stent and rarely within the graft itself. In-stent stenosis can be detected as focally increased (>250cm/s) or decreased (<50cm/s) velocities on Doppler ultrasound. TIPS thrombosis can present as echo­genic material within the graft and lack of ow on Doppler imaging. Angiography can be performed for conrmation and therapeutic intervention. Acute thrombosis of the stent can be treated with mechanical thrombectomy or catheter­directed thrombolysis. Chronic thrombus can be addressed with angioplasty or restenting, with the latter option result­ing in lower recurrence rates. In the era of PTFE stent grafts:
• Two-year primary patency is approximately 76% and
diminishes to 50% at 6years [42].
• Secondary patency at 6 years is approximately 84%
[7, 43].
TIPS can exacerbate preexisting liver disease by shunting portal blood ow away from the hepatic parenchyma. Increasing serum transaminases, bilirubin, and INR are sug­gestive of worsening liver function. Higher baseline MELD scores are associated with an increased incidence of post­TIPS liver failure [44]. Appropriate patient selection and accepting a higher post-TIPS portosystemic gradient in patients with MELD >14 can help to minimize this risk [45]. Similar to hepatic encephalopathy, TIPS reduction/occlusion can be performed in cases where conservative measures fail. In severe cases, liver transplantation may be required.
Key Point
First-line therapy for hepatic encephalopathy is oral lactulose titrated to 2–3 bowel movements a day.
Key Point
TIPS stenosis can be detected on US with >250 or
<50 cm/s in-stent velocities, and most commonly
occurs in the unstented segment of hepatic vein adja-
cent to the TIPS.
426
R. Koppula and Z. J Haskal

References

1. CDCData [Internet]. [cited 2017 Feb 3]. Available from: https://
www.cdc.gov/nchs/data/nvsr/nvsr65/nvsr65_04.pdf.
2. Berzigotti A, Seijo S, Reverter E, Bosch J. Assessing portal hypertension in liver diseases. Expert Rev Gastroenterol Hepatol. 2013;7(2):141–55.
3. Groszmann RJ, Wongcharatrawee S. The hepatic venous pressure gradient: anything worth doing should be done right. Hepatology (Baltimore, MD). 2004;39(2):280–2.
4. Garcia-Tsao G, Groszmann RJ, Fisher RL, Conn HO, Atterbury CE, Glickman M. Portal pressure, presence of gastroesopha­geal varices and variceal bleeding. Hepatology (Baltimore, MD). 1985;5(3):419–24.
5. Merkel C, Bolognesi M, Bellon S, Zuin R, Noventa F, Finucci G, et al. Prognostic usefulness of hepatic vein catheterization in patients with cirrhosis and esophageal varices. Gastroenterology. 1992;102(3):973–9.
6. Berzigotti A, Rossi V, Tiani C, Pierpaoli L, Zappoli P, Riili A, etal. Prognostic value of a single HVPG measurement and Doppler­ultrasound evaluation in patients with cirrhosis and portal hyper­tension. JGastroenterol. 2011;46(5):687–95.
7. Merkel C, Marin R, Sacerdoti D, Donada C, Cavallarin G, Torboli P, etal. Long-term results of a clinical trial of nadolol with or without isosorbide mononitrate for primary prophylaxis of variceal bleed­ing in cirrhosis. Hepatology (Baltimore, MD). 2000;31(2):324–9.
8. Groszmann RJ, Garcia-Tsao G, Bosch J, Grace ND, Burroughs AK, Planas R, etal. Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis. N Engl JMed. 2005;353(21):2254–61.
9. Bosch J, Pizcueta P, Feu F, Fernández M, García-Pagán JC. Pathophysiology of portal hypertension. Gastroenterol Clin N Am. 1992;21(1):1–14.
10. Gupta TK, Chen L, Groszmann RJ. Pathophysiology of portal hypertension. Clin Liver Dis. 1997;1(1):1–12.
11. García-Pagán J-C, Gracia-Sancho J, Bosch J.Functional aspects on the pathophysiology of portal hypertension in cirrhosis. JHepatol. 2012;57(2):458–61.
12. Iwakiri Y, Groszmann RJ.The hyperdynamic circulation of chronic liver diseases: from the patient to the molecule. Hepatology (Baltimore, MD). 2006;43(2 Suppl 1):S121–31.
13. Ginés P, Quintero E, Arroyo V, Terés J, Bruguera M, Rimola A, etal. Compensated cirrhosis: natural history and prognostic factors. Hepatology (Baltimore, MD). 1987;7(1):122–8.
14. Ginès P, Fernández-Esparrach G, Arroyo V, Rodés J.Pathogenesis of ascites in cirrhosis. Semin Liver Dis. 1997;17(3):175–89.
15. Solà E, Ginès P. Renal and circulatory dysfunction in cirrhosis: current management and future perspectives. J Hepatol. 2010; 53(6):1135–45.
16. AASLDPracticeGuidelineAsciteDuetoCirrhosisUpdate 2012Edition4_.pdf [Internet]. [cited 2017 Mar 1]. Available from: http://www.aasld.org/sites/default/les/guideline_documents/
AASLDPracticeGuidelineAsciteDuetoCirrhosisUpdate 2012Edition4_.pdf.
17. Grace ND.Prevention of initial variceal hemorrhage. Gastroenterol Clin N Am. 1992;21(1):149–61.
18. Smith JL, Graham DY.Variceal hemorrhage: a critical evaluation of survival analysis. Gastroenterology. 1982;82(5 Pt 1):968–73.
19. Garcia-Tsao G, Sanyal AJ, Grace ND, Carey WD. The practice guidelines Committee of the American Association for the study of liver diseases and the practice parameters Committee of the American College of Gastroenterology. Prevention and manage­ment of gastroesophageal varices and variceal hemorrhage in cirrhosis. Am JGastroenterol. 2007;102(9):2086–102.
20. Sharma M, Rameshbabu CS.Collateral pathways in portal hyper­tension. JClin Exp Hepatol. 2012;2(4):338–52.
21. Rösch J, Hanafee WN, Snow H.Transjugular portal venography and radiologic portacaval shunt: an experimental study. Radiology. 1969;92(5):1112–4.
22. Salerno F, Cammà C, Enea M, Rössle M, Wong F.Transjugular intra­hepatic portosystemic shunt for refractory ascites: a meta-analysis of individual patient data. Gastroenterology. 2007;133(3):825–34.
23. Garcia-Tsao G, Bosch J. Management of varices and variceal hemorrhage in cirrhosis. N Engl JMed. 2010;362(9):823–32.
24. Vangeli M, Patch D, Burroughs AK.Salvage tips for uncontrolled variceal bleeding. JHepatol. 2002;37(5):703–4.
25. Patidar KR, Sydnor M, Sanyal AJ.Transjugular intrahepatic porto­systemic shunt. Clin Liver Dis. 2014;18(4):853–76.
26. Boyer TD, Haskal ZJ.The role of transjugular intrahepatic porto­systemic shunt (TIPS) in the management of portal hypertension: update 2009. Hepatology. 2010;51(1):306.
27. Malinchoc M, Kamath PS, Gordon FD, Peine CJ, Rank J, ter Borg PC.A model to predict poor survival in patients undergoing tran­sjugular intrahepatic portosystemic shunts. Hepatology (Baltimore, MD). 2000;31(4):864–71.
28. Kamath PS, Wiesner RH, Malinchoc M, Kremers W, Therneau TM, Kosberg CL, et al. A model to predict survival in patients with end-stage liver disease. Hepatology (Baltimore, MD). 2001; 33(2):464–70.
29. Singal AK, Kamath PS. Model for end-stage liver disease. JClin Exp Hepatol. 2013;3(1):50–60.
30. Ferral H.The evaluation of the patient undergoing an elective tran­sjugular intrahepatic portosystemic shunt procedure. Semin Interv Radiol. 2005;22(4):266–70.
31. Ferral H, Gamboa P, Postoak DW, Albernaz VS, Young CR, Speeg KV, etal. Survival after elective transjugular intrahepatic portosys­temic shunt creation: prediction with model for end-stage liver disease score. Radiology. 2004;231(1):231–6.
32. Montgomery A, Ferral H, Vasan R, Postoak DW.MELD score as a predictor of early death in patients undergoing elective transjugu­lar intrahepatic portosystemic shunt (TIPS) procedures. Cardiovasc Intervent Radiol. 2005;28(3):307–12.
33. Fidelman N, Kwan SW, LaBerge JM, Gordon RL, Ring EJ, Kerlan RK.The Transjugular intrahepatic portosystemic shunt: an update. Am JRoentgenol. 2012;199(4):746–55.
34. Bai M, Qi X, Yang Z, Yin Z, Nie Y, Yuan S, etal. Predictors of hepatic encephalopathy after transjugular intrahepatic portosystemic shunt in cirrhotic patients: a systematic review. JGastroenterol Hepatol. 2011;26(6):943–51.
35. Sanyal AJ, Genning C, Reddy KR, Wong F, Kowdley KV, Benner K, etal. The North American study for the treatment of refractory ascites. Gastroenterology. 2003;124(3):634–41.
36. Garcia-Pagán JC, Heydtmann M, Raffa S, Plessier A, Murad S, Fabris F, et al. TIPS for Budd-Chiari syndrome: long-term results and prognostics factors in 124 patients. Gastroenterology. 2008;135(3):808–15.
37. Rössle M, Olschewski M, Siegerstetter V, Berger E, Kurz K, Grandt D. The Budd-Chiari syndrome: outcome after treatment with the transjugular intrahepatic portosystemic shunt. Surgery. 2004;135(4):394–403.
38. Dariushnia SR, Haskal ZJ, Midia M, Martin LG, Walker TG, Kalva SP, et al. Quality improvement guidelines for transjugu­lar intrahepatic portosystemic shunts. J Vasc Interv Radiol. 2016;27(1):1–7.
39. Madoff DC, Wallace MJ, Ahrar K, Saxon RR. TIPS-related hepatic encephalopathy: management options with novel endo­vascular techniques. Radiogr Rev Publ Radiol Soc N Am Inc. 2004;24(1):21–36–37.
40. Madoff DC, Wallace MJ. Reduced stents and stent-grafts for the management of hepatic encephalopathy after transjugular intrahepatic portosystemic shunt creation. Semin Interv Radiol. 2005;22(4):316–28.
38 Transjugular Intrahepatic Portosystemic Shunt (TIPS) andPortal Hypertension
427
41. Ferenci P. Hepatic encephalopathy—denition, nomenclature, diagnosis, and quantication: nal report of the working party at the 11th World Congresses of gastroenterology, Vienna, 1998. Hepatology. 2002;35(3):716–21.
42. Weber CN, Nadolski GJ, White SB, Clark TWI, Mondschein JI, Stavropoulos SW, et al. Long-Term Patency and Clinical Analysis of Expanded Polytetrauoroethylene-Covered Transjugular Intrahepatic Portosystemic Shunt Stent Grafts. J Vasc Interv Radiol JVIR. 2015;26(9):1257–1265; quiz 1265.
43. Suhocki P, Lungren M, Kapoor B, Kim C.Transjugular intrahepatic portosystemic shunt complications: prevention and management. Semin Interv Radiol. 2015;32(2):123–32.
44. Luca A, Miraglia R, Maruzzelli L, D’Amico M, Tuzzolino F.Early liver failure after transjugular intrahepatic portosystemic shunt in patients with cirrhosis with model for end-stage liver disease score of 12 or less: incidence, outcome, and prognostic factors. Radiology. 2016;280(2):622–9.
45. Chung H-H, Razavi MK, Sze DY, Frisoli JK, Kee ST, Dake MD, et al. Portosystemic pressure gradient during transjugular intra­hepatic portosystemic shunt with Viatorr stent graft: what is the critical low threshold to avoid medically uncontrolled low pres­sure gradient related complications? J Gastroenterol Hepatol. 2008;23(1):95–101.
Balloon-Occluded Transvenous Obliteration forGastric Varices
RonC.Gaba, NasyaMendoza-Elias, JohnH.Schilling, andAndrewJ.Lipnik

Pathophysiology

Etiology
Gastric varices (GVs) are abnormally dilated submucosal veins that may develop in patients with portal hypertension and which present a signicant risk of upper gastrointestinal (GI) bleeding. GVs arise as a part of the collateral circulation bypassing the portal venous system and result from the shift­ing hemodynamics seen in portal hypertension. GVs can develop from any cause of portal hypertension, including liver cirrhosis, non-cirrhotic portal brosis, extra-hepatic portal vein obstruction, and hepatic venous outow obstruction [1]. They may also arise from localized “left-sided” portal hypertension caused by splenic vein thrombosis (or, more rarely, splenic vein compression or stenosis). This left-sided portal hypertension usually occurs in the setting of pancre­atitis, local neoplasm, or other pancreatic disease [2]. Finally, GVs may arise secondary to therapeutic obliteration of esophageal varices (EVs) [1].
39
morbidity, mortality, rebleeding rates, and transfusion requirements [3]. Mortality at 6weeks after a bleed may be as high as 20% [4] and 2-year mortality related to GV bleed­ing approaches 45% [1].
Independent risk factors for bleeding from GVs include fundal location, red color spots on endoscopy, diameter larger than 5mm, and higher Child-Pugh class [5]. An ele­vated portosystemic pressure gradient exceeding 12mm Hg is a known risk factor for bleeding in EVs. However, this relationship is more complex in GVs due to the high preva­lence of spontaneous left-sided portosystemic shunts in these patients, and GVs are thought to bleed at lower portosys­temic gradients as compared to EVs [68], with a signicant proportion purported to bleed at portosystemic gradients below the recognized 12mm Hg threshold [4].
Key Point
Child-Pugh classication for the severity of cirrhosis is based on:
• Encephalopathy
Epidemiology andBleeding Risk
GVs occur in approximately 20% of patients with portal hypertension [1] and are typically discovered through screen­ing of cirrhotic patients or during management of an acute upper GI bleed. The overall 2-year bleeding incidence for GVs is estimated to be around 25%, with some variation depending on GV subtype [1]. While GVs bleed with a lower incidence than EVs [1], GV bleeding events are generally more severe than EV bleeds and are associated with higher
R. C. Gaba (*) · N. Mendoza-Elias · J. H. Schilling · A. J. Lipnik University of Illinois Hospital, Department of Radiology, Chicago, IL, USA e-mail: rgaba@uic.edu; nmendo2@uic.edu; alipnik@uic.edu
© Springer International Publishing AG, part of Springer Nature 2018 N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_39
• Ascites
• Bilirubin
• Albumin
• Prolonged PT or elevated INR
Key Point
Risk factors for gastric varices bleeding:
• Fundal location
• Red color spots on endoscopy
• Diameter>5mm
• Higher Child-Pugh class
429
430
R. C. Gaba et al.
Table 39.1 Kiyosue classication of GV inow and outow [10]
Anatomic type Description Inow Type 1 Single inow vessel (LGV, PGV, or SGV) Type 2 More than one inow vessel (LGV, PGV, and/or
SGV) Type 3 Direct splenorenal shunt Outow Type A Single outow (GRS) Type B Dominant GRS plus collaterals (B1, low ow
collaterals; B2, medium ow collaterals; B3, high
ow collaterals) Type C GRS plus gastrocaval shunt
GV gastric variceal, LGV left gastric vein, PGV posterior gastric vein, SGV short gastric vein, GRS gastrorenal shunt
however, fundal GVs (GEV2 and IGV1) have a much higher bleeding incidence (55–78%) compared with GEV1 and IGV2 (both around 10%) [1]. Fundal GVs therefore should be considered high risk and important targets for therapeutic intervention.
Fig. 39.1 Sarin classication scheme for GVs (Illustration by Janet
Sinn-Hanlon, DesignGroup@VetMed)
Anatomic Classication
The most widely utilized classication system for gastric varices was proposed by Sarin etal. [1], who prospectively studied patients with portal hypertension and classied GVs into four groups (Fig.39.1):
1. Type 1 gastroesophageal varices (GEV1): continuous varices extending from the esophagus down the cardia or lesser curvature of the stomach (74%).
2. Type 2 gastroesophageal varices (GEV2): continuous, often tortuous, varices extending from the esophagus toward the gastric fundus (21%).
3. Type 1 isolated GVs (IGV1): isolated gastric fundal vari­ces that are often tortuous (4%).
4. Type 2 isolated GVs (IGV2): ectopic varices in other areas of the stomach including the antrum, body, and/or pylorus (2%).
In general, EVs occur more frequently than GVs in cirrhotic
patients (approximately 60% versus 40% incidence) [9]. Among GVs, GEV1 are the most common GV type (74%) [1];
GV Filling andDrainage
GV inow and outow may be classied using the Kiyosue classication scheme [10] (Table 39.1). In general, GV inow occurs via combinations of the left gastric, posterior gastric vein, and short gastric veins, with outow via gastro­renal and gastrocaval shunts, as well as collateral vessels (e.g., phrenic veins) (Figs.39.2 and 39.3). Typically, GEV1 and EVs ll primarily via the left gastric vein, which nor­mally ows into the portal vein but may ow cephalad into the azygous system due to portal hypertension [9, 11]. Fundal GVs (GEV2 and IGV1) typically arise from the posterior gastric vein and short gastric veins (which normally drains into the splenic vein), with variable contribution by the left gastric vein [9, 11]. Importantly, most fundal GVs occur in conjunction with spontaneous left-sided gastrorenal or sple­norenal shunts to the left renal vein [3, 9]. These shunts are more common with GVs than EVs and may increase risk of hepatic encephalopathy in these patients [11]. IGV2 are less common and lower-risk varices that may arise from branches of the gastroepiploic veins [4].

Clinical Indication

Physical Exam andImaging Findings
Patients at higher risk for developing GVs will display pathognomonic signs of portal hypertension secondary to chronic liver disease. These signs include splenomegaly, spi­der nevi, jaundice with scleral icterus and palmar erythema,
39 Balloon-Occluded Transvenous Obliteration forGastric Varices
Fig. 39.2 Anatomic diagram
of GV inow and outow. PV portal vein, SV splenic vein, MV mesenteric vein, LGV left gastric vein, PGV posterior gastric vein, SGV short gastric vein, GV complex gastric variceal complex, GRS gastrorenal shunt, LRV left renal vein, GCS gastrocaval shunt, IVC inferior vena cava (Illustration by Janet Sinn-Hanlon, DesignGroup@VetMed)
Fig. 39.3 Portal venogram
(a) performed in 74-year-old man with IGV1 demonstrates inow via the left gastric vein (black arrow), posterior gastric vein (white arrowheads), and short gastric veins (black arrowheads) (Kiyosue type 2). Delayed image after portal venogram (b) performed in 53-year-old woman with IGV1 displays outow via gastrorenal shunt (arrow) (Kyosue type A). Short gastric venogram (c) performed in 56-year-old woman with IGV2 depicts typical “pinch point” narrowing (arrow) at the lower gastrorenal shunt, which is useful for lodging occlusion balloon during BRTO.
431
432
R. C. Gaba et al.
ascites, caput medusa, and hepatic encephalopathy. The presence of varices is thought to correlate with the severity of liver dis­ease. This is substantiated by the fact that 40% of Child-Pugh class A patients develop varices, while 85% of Child-Pugh class C patients develop varices (refer to Chap. 38 for more information on Child-Pugh classication). Before rupture, GVs can manifest endoscopic ndings of variceal red spots, possibly accompanied by red wale marks (vertical red streaks at the surface of the varix, resembling a red version of the wales of corduroy pants) or portal gastropathy. On imaging, GVs manifest as contrast-enhancing serpiginous submucosal structures abutting the stomach (Fig. 39.4).
While GVs may be clinically silent, the most serious clinical presentation is that of life-threatening bleeding due to rupture of the friable and fragile supercial ectatic vessels visible through the thin gastric mucosal layer (see Fig.39.4).
Key Point
Signs of chronic liver disease:
• Splenomegaly
• Spider nevi
• Jaundice
• Scleral icterus
• Ascites
• Caput medusa
• Hepatic encephalopathy
Indications forTreatment
Medical treatment of GVs is indicated for small (<5 mm) varices in a high-risk setting (Child-Pugh class B/C or red wale marks on endoscopy) and for large (>5mm) varices, even in a low-risk setting (Child-Pugh A, no red wale marks on endoscopy) [12]. Interventional treatment of GVs should be considered in the presence of large (>5mm) varices in a high-risk setting (Child-Pugh class B/C or red wale marks on endoscopy) or in the case of acute bleeding or recurrent hemorrhage [12].
Fig. 39.4 A 50-year-old man with IGV1. Axial contrast-enhanced CT
image (a) demonstrates submucosal GV complex (arrow) in the gastric fundus. Endoscopic image (b) shows GV (arrow), which exhibits active bleeding

Conventional Therapy

Medical Management
The goal of medical management of GVs is to maintain the hepatic venous pressure gradient (HVPG) below 12mm Hg or prevent it from increasing more than 10% from the patient’s baseline [12]. The noninvasive gold standard for achieving this goal and managing varices to prevent rupture and subsequent bleeding is the use of nonselective beta­blocker medications. Any traditional beta-blocker, such as propranolol or nadolol, can be used, but carvedilol has been shown to be the most effective at lowering HVPG [12]. HVPG surpassing 10 mm Hg is a signicant indicator of increased risk of complications, including being the stron­gest predictor of variceal development. HVPGs of 12mm Hg or greater, or a greater than 10% increase from baseline, should merit further endoscopic surveillance, as should platelets dropping below 150,000 per mL, or a transient elastography measure of liver stiffness greater than 20kPa on two separate occasions [13].
39 Balloon-Occluded Transvenous Obliteration forGastric Varices
Key Point
Hepatic venous pressure gradient >10 is a signicant predictor of variceal development.
Surgical Management
After peaking in use during the 1970s and 1980s, surgical management is no longer widely employed in standard prac­tice for portal hypertension because of the advent and matura­tion of considerably less invasive techniques for emergent variceal bleeding control, resulting in long-term improvement [14]. The only standard surgical treatment of portal hyperten­sion and liver disease is liver transplantation. But, operative portosystemic shunt creation via side-to-side portocaval shunts, mesocaval with interposition H- or C-graft shunts, and splenorenal shunts are also potential surgical interven­tions for management [15].
Endoscopists routinely treat GV bleeds via endoscopic
sclerotherapy and endoscopic obturation with n-2-butyl­cyanoacrylate. These methods are routinely used for rst time GV bleeds and effectively obtain initial hemostasis in more than 90% of cases [16]. Endoscopic sclerotherapy and endoscopic glue obturation are preferred to endoscopic band ligation of GVs due to lower recurrent hemorrhage rates [12, 17]. Minnesota or Sengstaken-Blakemore tubes may be employed for temporary balloon tamponade of acute refractory GV bleeding for up to 24h. These provide temporary control to allow planning of the best denitive intervention.
433

Interventional Therapy

Transjugular intrahepatic portosystemic shunt (TIPS) cre­ation is generally employed for prevention of recurrent hem­orrhage in cases of intolerance or resistance to medical and endoscopic treatment or as rescue therapy in cases of refrac­tory acute bleeding (refer to Chap. 38 for more information) [1820]. Moreover, TIPS may be used as rst-line therapy for GVs in the absence of endoscopic sclerotherapy or endo­scopic glue obturation materials or expertise [12]. TIPS with or without GV embolotherapy using metallic coils and/or plugs is associated with initial bleeding control in more than 90% of cases [2123] and is associated with lower rebleed­ing rates than ES and endoscopic glue obturation [22]. Despite initial bleeding cessation, GV recurrent hemorrhage rates after TIPS may range between 13% and 53% [7, 24], and clinical outcomes are generally thought to be inferior to TIPS with or without embolotherapy for EVs, which show rebleeding rates ranging from 11% to 22% [7, 24].
Balloon-occluded retrograde transvenous obliteration (BRTO) of varices was pioneered in the 1970s, initially employing an antegrade transhepatic or trans-splenic approach. In 1984, Olson etal. reported the rst case utilizing a balloon placed into a gastrorenal shunt via a transfemoral approach to arrest ow and reux a sclerosing agent retro­grade into GVs [25]. In the 1990s, Kanagawa coined the term balloon-occluded retrograde transvenous obliteration (BRTO) and further established the basic approach currently in use [26, 27] (Fig.39.5). The procedure has subsequently evolved to be the primary procedural treatment for bleeding GVs in Japan, with variations gaining popularity in the United States and Europe over the past decade.
Fig. 39.5 Anatomic diagram
depicting BRTO concept, with occlusion balloon and coaxial microcatheter advanced via the gastrorenal shunt for obliteration of GV complex. PV portal vein, SV splenic vein, MV mesenteric vein, LGV left gastric vein, PGV posterior gastric vein, SGV short gastric vein, GV complex gastric variceal complex, GRS gastrorenal shunt, LRV left renal vein, GCS gastrocaval shunt, IVC inferior vena cava. Illustration by Janet Sinn-Hanlon, DesignGroup@VetMed
434
Table 39.2 Treatment approach to GVs in different clinical or anatomic
scenarios [30]
Clinical or Anatomic Scenario Treatment GVs BRTO GVs+hepatic encephalopathy BRTO GVs+ascites/hydrothorax BRTO±TIPS GVs+uncontrolled EVs BRTO+TIPS GVs+splenic vein thrombosis BRTO+splenic artery
embolization
GVs+portal vein thrombosis BRTO + portal vein
recanalization-TIPS
GVs gastric varices, BRTO balloon-occluded retrograde transvenous obliteration, TIPS transjugular intrahepatic portosystemic shunt, EVs esophageal varices
BRTO has an accepted role for treatment of GVs, espe­cially in patients with poor hepatic reserve (model for end­stage liver disease or MELD score exceeding 18), hepatic encephalopathy, and/or heart failure in whom TIPS is con­traindicated. BRTO indications include GVs that are actively, previously, or at high risk for bleeding. GV oblit­eration may be combined with other procedures depending on the particular clinical and anatomic scenario (Table39.2) or based on operator preference. Notably, BRTO of GVs can help resolve hepatic encephalopathy, if present, through physiologic portosystemic shunt closure. Contraindications to BRTO include lack of a gastrorenal shunt or other systemic access to GVs, as well as portal and/or splenic vein throm­bosis in the absence of alternative mesenteric or splenic venous outow (which risks mesenteric and splenic isch­emia and infarction). Pre-procedure patient evaluation includes a thorough history and physical exam, laboratory evaluation, and upper endoscopy to diagnose and conrm the presence of GVs. Triple-phase contrast-enhanced cross­sectional imaging is routinely obtained to delineate GV anatomy (including inow and outow vessels) (Fig.39.6) for pre-procedure planning.
R. C. Gaba et al.
The How To
1. Systemic venous access: Systemic venous access is gained via a common femoral vein (CFV) or internal jugular vein (IJV) approach via the Seldinger tech­nique (refer to Chap. 8 for more information). The choice of access vein depends on the orientation of the left renal vein and the distance between the ori­gins of the left renal vein and gastrorenal shunt, as well as operator preference. A sheath large enough to accommodate an appropriate-sized occlusion bal­loon is placed into the inferior vena cava (IVC).
2. Gastrorenal shunt cannulation: The left renal vein is selected with an angled catheter and guidewire (if approached from the CFV) or a reverse curved catheter (if approached from the IJV). The gastrore­nal shunt is then selected by gently probing the cra­nial aspect of the left renal vein. The gastrorenal shunt is cannulated more deeply in anticipation of placing an occlusion balloon.
3. Balloon-occluded retrograde venogram (BORV): The catheter is exchanged for an appropriately sized compliant occlusion balloon, which is typi­cally lodged at a “pinch point” above the common stump of the gastrorenal shunt and left adrenal vein.
­rial (or carbon dioxide in patients with a contrast allergy or renal failure) is gently injected by hand to
39.6). The venogram is
veins (typically posterior gastric vein and/or short gastric veins).
4.
-
Key Point
MELD score is calculated using the patient’s values for:
• Bilirubin.
• Creatinine.
• INR.
• MELD 18 indicates poor hepatic reserve.
(e.g., inferior phrenic vein, gastrocaval shunts) are embolized using metallic coils, plugs, gelatin sponge, or sclerosant. After embolization, repeat BORV is performed to ensure visualization of the GVs and
5. Sclerosant foam preparation: Once the GVs are
located in the GV proper. The sclerosant foam is mixed; the most frequently used sclerosant is 3% sodium tetradecyl sulfate, which is mixed with air to create a foam, increasing surface contact area with