肝移植术后门静脉并发症的发生（图文演示）

PORTAL VEIN COMPLICATIONS AFTER LIVER TRANSPLANTATION

JP Lerut, MD, PhD , Université Catholique de Louvain, Brussels, Belgium


中文版：肝移植术后门静脉并发症的发生（中文图文）

1. Portal vein thrombosis (PVT)

                               
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1.1. IncidencePortal vein thrombosis (PVT) after liver transplantation is rare. An overall incidence of 1 to 2% has been reported; this complication is more frequent in pediatric liver transplantation (LT) (2 to 14%).
1.2. EtiologyPredisposing factors to the development of PVT have been identified, such as donor-recipient size mismatch, recipient portal vein thrombosis and hypoplasia, large portosystemic collaterals, previous splenectomy and pre-existing, especially non-selective, portosystemic shunts.
The higher incidence of PVT in pediatric liver transplantation is due primarily to inappropriate surgical technique. Discrepancy between donor and recipient portal veins when using reduced size or split liver grafts can be overcome by longitudinal plasty and coning on the graft site and by using the recipient portal vein bifurcation or finally by making the anastomosis on the spleno-mesenteric junction.
In case of severe portal vein hypoplasia, it is better to directly anastomose the portal vein (PV) of the graft to the superior mesenteric vein (SMV). Interposition of a free iliac vein graft is many times necessary to bridge the gap between SMV and donor portal vein.
Attention must be given in these cases to avoid PV compression behind the reduced or split liver graft. This can be avoided by temporarily closing the abdomen with a prosthetic graft.

[点击按纽展开更多->收起->回放] The use of split and reduced size liver grafts enhances the incidence of vascular complications e.g. kinking of portal vein due to incongruity of graft and pediatric abdominal cavity	[点击按纽展开更多->收起->回放] Intraoperative view showing mechanisms of compression of portal vein at end of graft implantation
[点击按纽展开更多->收起->回放] This problem can be solved by construction of a straight connection between SMV and the umbilical portion of the allograft’s portal vein (Rex’s recessus)

Incidence of PVT after liver transplantation in patients having preoperative splanchnic venous thrombosis ranges from 3 to 28.5%. The key to avoid PVT in these patients is to decide on the method of portal vein reconstruction before starting the implantation of the graft. Obstruction of the venous inflow can usually (nearly always) be completely relieved by eversion thrombectomy. If the PVT extends to the SMV or if the PV has been reduced to a fibrotic vessel remnant, an infra-colic approach must be opted for using an iliac venous homograft to join donor PV and SMV. Sometimes, anastomosis between donor PV and recipient splanchnic system is impossible. Intraoperative venography through ileocolic or inferior mesenteric veins may be helpful in order to properly assess venous anatomy. Successful restoration of the portal allograft perfusion has been obtained by anastomosing donor PV to left gastric, hepatoduodenal, choledochal, gastroepiploic and ileo-colic varices and even by (partial) arterialization of the portal vein.

[点击按纽展开更多->收起->回放] Eversion thrombectomy of portal vein and superior mesenteric vein (SMV)

[点击按纽展开更多->收起->回放] Thrombectomy specimen

In case of complete splanchnic venous thrombosis, the allograft can only be vascularized by performing either a combined liver intestinal transplant or a cavo-portal transposition. The latter intervention, which is much less invasive consists of an interruption of the caval flow in order to deviate it into the portal vein. Incomplete decompression of the splanchnic venous system may lead to post-transplant rupture of gastric or esophageal varices. Elastic banding, and eventually splenic artery embolization or splenectomy may be necessary to treat this complication.
Adequacy of portal allograft perfusion should be assessed by electromagnetic flow measurement (EFM). This may be of utmost importance in cases of extended splanchnic thrombosis and in the presence of pronounced venous collaterals or surgical distal splenorenal shunt. In our experience, it has never been necessary to interrupt collaterals or to dismantle a splenorenal shunt in such cases. It should be reminded that both surgical maneuvers are not without risk.
1.3. DiagnosisPVT can be easily detected by routine Doppler ultrasound (DUS) examination.
1.4. Clinical presentation and treatmentAcute PVT can present as severe graft dysfunction, liver failure, massive ascites, intestinal congestion and even gastrointestinal bleeding. Early diagnosis usually allows early and prompt surgical re-intervention. Early thrombectomy is successful in most of the cases; in some patients it is still necessary to proceed with an urgent liver re-transplantation (re-LT).
Early PVT can now be treated successfully non-operatively using interventional radiological techniques. Access to the portal vein to deliver local thrombolytic agents can be obtained via a percutaneous transhepatic or transjugular intrahepatic approach.

[点击按纽展开更多->收起->回放] Early post-transplant portal vein thrombosis	[点击按纽展开更多->收起->回放] Early post-transplant portal vein thrombosis
[点击按纽展开更多->收起->回放] Early post-transplant portal vein thrombosis using a previously created TIPS-channel

When the portal venous thrombosis causes acute liver failure, urgent re-transplantation is always necessary.
In case of late PVT, the treatment depends upon the clinical presentation. This presentation is similar to the non-transplant setting of PVT. Sclerotherapy of bleeding varices is worthwhile but usually a more definitive treatment of the portal hypertension will be necessary.
Development of symptomatic portal hypertension can be treated using selective or non-selective portosystemic shunting (meso-caval H-graft shunt or distal splenorenal shunt). Interposition of a venous graft between the umbilical portion of the left portal vein (meso-rex shunt following de Ville de Goyet) and the SMV has now become the preferable option as it restores a physiologic splanchnic flow to the allograft.

[点击按纽展开更多->收起->回放] Late post-transplant PVT and cavernomatous transformation	[点击按纽展开更多->收起->回放] This problem can be overcome using an interposition (preferably homologous) venous graft between SMV and patient left portal vein at Rex’s recessus (de Ville de Goyet shunt)
[点击按纽展开更多->收起->回放] CT scan showing patent vascular prosthesis at Rex’s recessus	[点击按纽展开更多->收起->回放] Doppler ultrasound showing patent vascular prosthesis at Rex’s recessus

Late PVT has also been successfully treated by means of local thombolytic therapy and percutaneous angioplasty.

2. Portal vein (PV) stenosis

                               
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PV stenosis can be responsible for (recurrent) variceal bleeding and/or liver dysfunction. This diagnosis can be easily made by DUS examination. Therapy mainly consists of interventional radiology using placement of an endovascular metallic stent.

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3. Left-sided portal hypertension and splenic vein thrombosis (SpVT)

                               
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Surgical bypassing or opening of thrombosed segments of recipient PV are now extensively used in clinical practice.
Unrecognized thrombosis or clotting of the proximal part of the splenic vein (SpV) may prevent adequate decompression of the left epigastric splanchnic bed. This might cause left-sided portal hypertension, which might be responsible for the rupture of esophageal and/or gastric varices in the presence of a patent allograft PV.
Esophageal or gastric variceal bleeding in the presence of patent PV mandates prompt angiographic study to differentiate PV from SpVT. In addition to gastric varices, esophageal varices may be present depending on the drainage of the coronary vein. If the coronary vein drains into the portal vein (which happens in 24% of cases), esophageal veins can be decompressed; if the coronary vein drains into the splenic vein (17%), esophageal veins will not be decompressed and can develop into varices. In 49% of cases, the coronary vein drains into the confluence of the portal vein and the splenic vein; decompression of the esophageal veins then depends on the extent of the SpVT.
Complicated left-sided post-LT portal hypertension can be solved in different ways. Sclerotherapy or elastic ligation of the ruptured varices can be done but do not take the underlying pathophysiological process into account. Splenectomy can represent a simple solution to gastric variceal bleeding secondary to SpVT, but it has important consequences in relation to infectious post-transplant complications.
A more physiological but more risky procedure may consist in the interposition of a free vein graft between the portal vein and a patent part of the SpV. This procedure necessitates dissection of the SpV in the presence of venous hypertension but offers the advantage of spleen preservation

4. Inferior vena cava complications of liver transplantation (LT)

                               
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4.1. Inferior vena cava stenosisThe largest vessels to be anastomosed in LT are the inferior vena cava (IVC) of the donor and recipient. Significant stenosis or thrombosis after LT is therefore a rare phenomenon. Stenosis or obstruction can be due to compression, kinking or twisting of the IVC, to erroneous placement of transjugular intrahepatic portosystemic shunts and to recurrent Budd-Chiari syndrome.

Because there may be a large overlap between the signs and symptoms of IVC stenosis or obstruction and other clinical syndromes, clinical diagnosis may be difficult. Doppler ultrasound (DUS) is a good screening tool for IVC occlusion, but is not very sensitive for detection of intrahepatic IVC stenosis. Angiography is necessary to define the nature, level, and extent of stenosis and obstruction more precisely.
Suprahepatic IVC stenosis presents with hepatomegaly, liver dysfunction, ascites, and edema and liver biopsy shows centrolobular congestion. In case of infrahepatic IVC stenosis peripheral limb and truncal edema, ascites and kidney failure may develop. Proteinuria and hematuria may also be present (Budd-Chiari-like syndrome).
In some cases, pulmonary embolism or acute liver graft failure may be the first signs of the IVC thrombosis.
Literature reports addressing the problem of IVC stenosis or obstruction are scarce. The Pittsburgh series showed that the existence of a pressure gradient of 8 cm of water or more across the caval anastomosis and injection of contrast material into the hepatic or renal veins was invariably associated with severe clinical symptoms. Symptoms can however also be present in case of pressure gradients of a few centimeters of water. All these patients required treatment using either surgical revision or interventional radiological techniques. Revision of suprahepatic IVC stenosis can be extremely difficult. Balloon angioplasty with intravascular expandable stent placement has proven to be a very good treatment of this complication resulting in the rapid improvement of symptoms. Careful follow-up remains necessary as re-stenosis after percutaneous balloon dilatation is frequent.
Infrahepatic IVC stenosis is more accessible to surgical treatment. Surgical or radiological approach is chosen according to patient’s condition and time period between transplantation and diagnosis of stenosis.

[点击按纽展开更多->收起->回放] Severe IVC stenosis at the level of the suprahepatic caval anastomosis	[点击按纽展开更多->收起->回放] Narrowing of IVC causing severe ascites and development of paracaval collaterals emptying into the azygos system, despite the presence of a gradient of 3 mm Hg only
[点击按纽展开更多->收起->回放] Refractory ascites was treated by placement of retrohepatic endovascular stent

4.2. Inferior vena cava thrombosisComplete IVC thrombosis after orthotopic liver transplantation (OLT) is a very rare event.
This complication is mostly related to the temporary occlusion of the IVC necessary to replace IVC in classical liver transplantation; other causes may be upward extension of deep femoral and iliac venous thrombosis, or hypercoagulable state of the recipient (Budd-Chiari syndrome, etc.). The IVC thrombosis is frequently confined to the lower infrarenal segment of the IVC; the increased caval blood flow at the level of the renal veins probably limits upward extension of the thrombus.
This complication can be resolved using interventional radiological techniques combining in situ thrombolysis and, if necessary, placement of an intravascular expandable stent.

[点击按纽展开更多->收起->回放] CT scan showing post-transplant ascites due to partial IVC thrombosis

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DUS and cavography show complete IVC thrombosis

5. Hepatic vein outflow obstruction

                               
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Hepatic venous stenosis or occlusion is a rare complication in whole liver grafting except in patients with pre-existing Budd-Chiari syndrome. This complication is mostly due to malpositioning of a partial graft in a cadaveric or living-related donor, or is due to inappropriate modified implantation techniques such as piggy-back and cavo-caval liver grafting.
Partial hepatic vein occlusion may be well tolerated due to compensatory hypertrophy of the remaining liver parenchyma. It may however sometimes give rise to refractory ascites.
If a complete hepatic venous outflow obstruction occurs, immediate re-transplantation is necessary. Partial symptomatic venous outflow obstruction is best treated by interventional radiology using balloon angioplasty and placement of an endovascular stent. In patients with good liver function and refractory ascites, meso-caval shunting can be the surgical alternative.

[点击按纽展开更多->收起->回放] Thrombosis of left hepatic vein (HV) and stenosis of middle HV responsible for massive ascites formation	[点击按纽展开更多->收起->回放] Stenosis of middle hepatic vein of right split liver graft
[点击按纽展开更多->收起->回放] Stenosis of middle hepatic vein of right split liver graft treated with endovascular stent placement	[点击按纽展开更多->收起->回放] Venography showing thrombosis of right hepatic vein causing refractory ascites

6. Conclusion
Vascular arterial and venous complications after liver transplantation can cause significant morbidity and mortality.
Early diagnosis using Doppler US screening confirmed with angiography, and prompt therapy using either surgical or interventional radiological procedures are necessary for graft and patient salvage. Adequate intraoperative judgment and precise surgical implantation techniques are the keys to avoid these often dramatic complications.

7. References

                               
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7.1. Portal vein thrombosisAbouJaoude MM, Grant DR, Ghent CN, Mimeault RE, Wall WJ. Effect of portasystemic shunts on subsequent transplantation of the liver. Surg Gynecol Obstet 1991;172:215-9.

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Marujo WC, Langnas AN, Wood RP, Stratta RJ, Li S, Shaw BW, Jr. Vascular complications following orthotopic liver transplantation: outcome and the role of urgent revascularization. Transplant Proc 1991;23:1484-6.

Mazzaferro V, Todo S, Tzakis AG, Stieber AC, Makowka L, Starzl TE. Liver transplantation in patients with previous portasystemic shunt. Am J Surg 1990;160:111-6.

Moreno Gonzalez E, Gomez R, Bonet H, Garcia I, Gonzalez-Pinto I, Loinaz C, Maffettone V. Liver transplantation in patients with a previous portasystemic shunt. Hepatogastroenterology 1993;40:593-5.

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Pinna AD, Lim JW, Sugitani AD, Starzl TE, Fung JJ. "Pants" vein jump graft for portal vein and superior mesenteric vein thrombosis in transplantation of the liver. J Am Coll Surg 1996;183:527-8.

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Shaked A, Busuttil RW. Liver transplantation in patients with portal vein thrombosis and central portacaval shunts. Ann Surg 1991;214:696-702.

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Stieber AC, Zetti G, Todo S, Tzakis AG, Fung JJ, Marino I, et al. The spectrum of portal vein thrombosis in liver transplantation. Ann Surg 1991;213:199-206.

Troisi R, Kerremans I, Mortier E, Defreyne L, Hesse UJ, de Hemptinne B. Arterialization of the portal vein in pediatric liver transplantation. A report of two cases. Transpl Int 1998;11:147-51.

Turrion VS, Mora NP, Cofer JB, Solomon H, Morris CA, Gonwa TA, et al. Retrospective evaluation of liver transplantation for cirrhosis: a comparative study of 100 patients with or without previous porto-systemic shunt. Transplant Proc 1991;23:1570-1.

Tzakis A, Todo S, Stieber A, Starzl TE. Venous jump grafts for liver transplantation in patients with portal vein thrombosis. Transplantation 1989;48:530-1.

Tzakis AG, Kirkegaard P, Pinna AD, Jovine E, Misiakos EP, Maziotti A, et al. Liver transplantation with cavoportal hemitransposition in the presence of diffuse portal vein thrombosis. Transplantation 1998;65:619-24.

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7.2. Portal vein thrombosis – treatmentBhattacharjya T, Olliff SP, Bhattacharjya S, Mirza DF, McMaster P. Percutaneous portal vein thrombolysis and endovascular stent for management of posttransplant portal venous conduit thrombosis. Transplantation 2000;69:2195-8.

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Cherukuri R, Haskal ZJ, Naji A, Shaked A. Percutaneous thrombolysis and stent placement for the treatment of portal vein thrombosis after liver transplantation: long-term follow-up. Transplantation 1998;65:1124-6.

de Bono DP, Pringle S, Underwood I. Differential effects of aprotinin and tranexamic acid on cerebral bleeding and cutaneous bleeding time during rt-PA infusion. Thromb Res 1991;61:159-63.

De Carlis L, Del Favero E, Rondinara G, Belli LS, Sansalone CV, Zani B, et al. The role of spontaneous portosystemic shunts in the course of orthotopic liver transplantation. Transpl Int 1992;5:9-14.

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Demertzis S, Ringe B, Gulba D, Rosenthal H, Pichlmayr R. Treatment of portal vein thrombosis by thrombectomy and regional thrombolysis. Surgery 1994;115:389-93.

Emond JC, Heffron TG, Whitington PF, Broelsch CE. Reconstruction of the hepatic vein in reduced size hepatic transplantation. Surg Gynecol Obstet 1993;176:11-7.

Guckelberger O, Bechstein WO, Langrehr JM, Kratschmer B, Loeffel J, Settmacher U, et al. Successful recanalization of late portal vein thrombosis after liver transplantation using systemic low-dose recombinant tissue plasminogen activator. Transpl Int 1999;12:273-7.

Margarit C, Lazaro JL, Charco R, Hidalgo E, Revhaug A, Murio E. Liver transplantation in patients with splenorenal shunts: intraoperative flow measurements to indicate shunt occlusion. Liver Transpl Surg 1999;5:35-9.

Marino IR, Esquivel CO, Zajko AB, Malatack J, Scantlebury VP, Shaw BW, et al. Distal splenorenal shunt for portal vein thrombosis after liver transplantation. Am J Gastroenterol 1989;84:67-70.

Rivitz SM, Geller SC, Hahn C, Waltman AC. Treatment of acute mesenteric venous thrombosis with transjugular intramesenteric urokinase infusion. J Vasc Interv Radiol 1995;6:219-23; discussion 224-8.

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Ryu R, Lin TC, Kumpe D, Krysl J, Durham JD, Goff JS, et al. Percutaneous mesenteric venous thrombectomy and thrombolysis: successful treatment followed by liver transplantation. Liver Transpl Surg 1998;4:222-5.

Scantlebury VP, Zajko AB, Esquivel CO, Marino IR, Starzl TE. Successful reconstruction of late portal vein stenosis after hepatic transplantation. Arch Surg 1989;124:503-5.

Shapiro RS, Varma CV, Schwartz ME, Miller CM. Splenorenal shunt closure after liver transplantation: intraoperative Doppler assessment of portal hemodynamics. Liver Transpl Surg 1997;3:641-2.

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Troisi R, Kerremans I, Mortier E, Defreyne L, Hesse UJ, de Hemptinne B. Arterialization of the portal vein in pediatric liver transplantation. A report of two cases. Transpl Int 1998;11:147-51.
7.3. Left-sided portal hypertensionRanjan D, Purser R, Jonas M, Yrizzary J, Borgeson M, Miller J, et al. Isolated splenic vein thrombosis as a cause of massive upper- gastrointestinal bleeding following orthotopic liver transplantation. Transplantation 1991;52:725-7.

Stevenson WC, Sawyer RG, Pruett TL. Recurrent variceal bleeding after liver transplantation--persistent left-sided portal hypertension. Transplantation 1992;53:493-5.
7.4. Inferior vena cava and hepatic vein complicationsBjerke RJ, Mieles LA, Borsky BJ, Todo S. The use of transesophageal ultrasonography for the diagnosis of inferior vena caval outflow obstruction during liver transplantation. Transplantation 1992;54:939-41.

Ciccarelli O, Goffette P, Danse E, Weber J, Lerut J. Hepatic vein obstruction due to hypertrophy of right split-liver adult allograft. Transpl Int 2001;14:270-3.

Kishi K, Sonomura T, Nishida N, Mitsuzane K, Kobayashi H, Juri M, et al. [Self-expandable metallic stent therapy for inferior vena cava obstruction secondary to malignancy: clinical observations]. Nippon Igaku Hoshasen Gakkai Zasshi 1994;54:389-98.

Klintmalm GB, Alivizatos PA, Husberg BS, Howard TK, Small AB, Goldstein RM, et al. Hepatic transplantation in a patient with mesoatrial shunt and occlusion of the inferior vena cava. Surgery 1990;107:220-3.

Kraus TW, Rohren T, Manner M, Otto G, Kauffmann GW, Herfarth C. Successful treatment of complete inferior vena cava thrombosis after liver transplantation by thrombolytic therapy. Br J Surg 1992;79:568-9.

Mathew AT, Talbot D, Hudson M, Manas D, Rose JD. Post-regraft supra-hepatic caval obstruction in liver transplantation: a successful outcome with expandable stents. A case report. Transpl Int 1998;11:66-8.

Merhav H, Bronsther O, Pinna A, Zajko A, Bron K. Significant stenosis of the vena cava following liver transplantation-- a six-year experience. Transplantation 1993;56:1541-5.

Rose BS, Van Aman ME, Simon DC, Sommer BG, Ferguson RM, Henry ML. Transluminal balloon angioplasty of infrahepatic caval anastomotic stenosis following liver transplantation: case report. Cardiovasc Intervent Radiol 1988;11:79-81.

Zajko AB, Claus D, Clapuyt P, Esquivel CO, Moulin D, Starzl TE, et al. Obstruction to hepatic venous drainage after liver transplantation: treatment with balloon angioplasty. Radiology 1989;170:763-5.