肝移植术后血管并发症：第一部分（图文演示）

Vascular complications after liver transplantation: part i

VASCULAR COMPLICATIONS AFTER LIVER TRANSPLANTATION

中文版：肝移植术后血管并发症：第一部分（中文图文演示）
JP Lerut, MD, PhD , Université Catholique de Louvain, Brussels, Belgium

1. Introduction
Advances in surgical techniques have contributed to the markedly improved results of liver transplantation (LT). Despite the development of better reconstructing methods of the hepatic artery (HA), portal vein (PV), hepatic venous outflow and bile ducts, about 10% of liver grafts are still lost due to vascular and biliary complications. Complications involving hepatic artery and portal vein are of special importance as they may immediately jeopardize the allograft as well as patient survival.
Graft and patient survival depend on early diagnosis of and prompt intervention on these complications.

2. Hepatic arterial complications after liver transplantation

                               
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2.1. Hepatic artery thrombosis
2.1.1. Incidence
Hepatic artery thrombosis (HAT) is one of most common serious problems after LT occurring in 1.6 to 8% of adults and 2.7 to 40% of children. These varying incidences reflect different means of diagnosis as well as the relative number of pediatric recipients within the different series. HAT represents a significant cause of graft and patient loss, especially in children transplantation; the overall mortality rate of HAT varies from 0 to 50%. About one quarter of children survive HAT without re-LT because of the rapid development of collateral arterial supply, which reconstitutes hepatic arterial inflow.

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Hepatic artery thrombosis (HAT)

2.1.2. Clinical presentation
The effect of interruption of arterial blood supply on a transplanted liver differs markedly from the effect of arterial interruption on a native liver. This is due to the absence of collaterals within the liver attachments and to the fact that the viability of the bile duct of the allograft depends entirely on the arterial peribiliary plexus.

The post-thrombosis course is manifested by a wide, time-dependent spectrum going from mild elevation of liver tests (transaminasemia and bilirubinemia) to extensive gangrene of the allograft.

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Angiography showing a complete stop at level of common hepatic artery

Early HAT presents with one of the four following syndromes:

• extensive hepatic infarction with potential development of acute hepatic failure. Radiographs may show intrahepatic gas formation.
  

  [点击按纽展开更多->收起->回放] Evolution of liver function test in massive liver necrosis		[点击按纽展开更多->收起->回放] Ultrasound showing inhomogeneous, hyperechogenic pattern corresponding to liver necrosis
  [点击按纽展开更多->收起->回放] Plain abdominal X-ray showing free gas at the right upper abdomen		[点击按纽展开更多->收起->回放] CT scan confirming gaseous gangrene of the left liver lobe and necrosis of the right liver lobe
  [点击按纽展开更多->收起->回放] CT scan confirming gaseous gangrene of the left liver lobe and necrosis of the right liver lobe		[点击按纽展开更多->收起->回放] Intraoperative view of necrosed liver
  [点击按纽展开更多->收起->回放] Hepatectomy specimen showing huge abscess formation of the right liver

• delayed biliary complications: cholangitis, biliary sepsis, leakage and strictures may present as late events of HAT. Leakage and strictures are secondary to ischemia of the distal donor bile duct.
  
  

  [点击按纽展开更多->收起->回放] HAT and biliary complications		[点击按纽展开更多->收起->回放] Percutaneous transhepatic cholangiography (PTC) showing biloma in continuity with bile duct
  [点击按纽展开更多->收起->回放] CT scan and hepatectomy specimen showing peripheral biloma of right liver		[点击按纽展开更多->收起->回放] CT scan and hepatectomy specimen showing peripheral biloma of right liver
  [点击按纽展开更多->收起->回放] Biloma of right liver drained percutaneously		[点击按纽展开更多->收起->回放] Histological examination of hepatectomy specimen showing necrosis of bile duct with dispersion of bile into surrounding tissue
  [点击按纽展开更多->收起->回放] High grade bilobar intrahepatic bile duct strictures at PTC		[点击按纽展开更多->收起->回放] High grade bilobar intrahepatic bile duct strictures at PTC treated with percutaneous balloon dilatation
  [点击按纽展开更多->收起->回放] Placement of endobiliary stents		[点击按纽展开更多->收起->回放] Intrahepatic ischemic type biliary tract lesions (IBTL) at PTC
  [点击按纽展开更多->收起->回放] Post-transplant evolution of biliary tree: despite normal early T-tube cholangiography, late PTC showed diffuse IBTL necessitating re-transplantation

  
  

• recurrent bacteremia frequently associated with intrahepatic abscess formation. The arterialized graft is especially vulnerable to invasion by intestinal micro-organisms, mainly Gram-negative bacteria. Formation of intrahepatic abscesses related to focal ductal ischemic necrosis is often associated with bile duct necrosis and later development of biliary strictures.
  
  

  [点击按纽展开更多->收起->回放] Liver function test with septicemia		[点击按纽展开更多->收起->回放] Pathways of graft infection
  [点击按纽展开更多->收起->回放] CT scan showing necrotic zone of right liver		[点击按纽展开更多->收起->回放] Necrotic zone of right liver corresponding on PTC with biloma
  [点击按纽展开更多->收起->回放] This lesion was present despite normal arterial signal at DUS		[点击按纽展开更多->收起->回放] Angiography explained the absence of DUS findings by showing extensive collateralization of hepatic artery thrombosis giving rise to a normal intrahepatic arterial tree
  [点击按纽展开更多->收起->回放] DUS showing normal intrahepatic arterial signal due to adequate collateralization in the presence of occlusion of the main HA trunk		[点击按纽展开更多->收起->回放] Right sectorial hepatic artery occlusion
  [点击按纽展开更多->收起->回放] Right sectorial hepatic artery occlusion responsible for localized liver necrosis on CT scan		[点击按纽展开更多->收起->回放] Liver necrosis secondary to right sectorial hepatic artery occlusion

  
  

• asymptomatic Doppler ultrasound (DUS) screening: HAT is fortuitously/accidentally diagnosed during routine postoperative DUS; liver tests may be normal or only mildly elevated.
  

Late HAT may be asymptomatic, found only on routine DUS or may be characterized by the development of single or multiple intrahepatic and/or extrahepatic bile duct strictures giving rise to relapsing bacteremia and cholangitis.
Changes in liver tests are frequently minimal due to collateralization originating from adhesions to diaphragm, retroperitoneum and other intra-abdominal viscera.

2.1.3. Etiology
HAT is probably the gravest post-transplant complication. A multitude of studies have been conducted to identify possible contributing factors of HAT:

• Technical/anatomical considerations:
  
  • arterial anatomical modification of the allograft supply, which is present in at least one third of cases,
    
    
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    Anatomical variants of hepatic arterial supply
    
  
  
  • median arcuate ligament compression of the celiac trunk,
  • intraoperative technical problems as e.g. intimal flap and media necrosis of donor hepatic artery; difficult site for arterial reconstruction and need for intraoperative revision of the anastomosis,
    
    
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    Angiography showing intimal flap at iliac conduit between hepatic artery and abdominal aorta
  • type of arterial reconstruction (end-to-end anastomosis vs. use of free iliac conduit interposition),
  • small (less than 3 mm) diameter of the hepatic artery,
  • type of donor liver (reduced size liver vs. whole liver in children),
  • size of donor (small liver from donor weighing less than 15 kg or being less than 2 years) or recipient (less than 15 kg or less than 2 years).
    
• Coagulation status:
  
  • hypercoagulable state related to antithrombin III deficiency or unknown Protein C or S deficiency,
  • presence of anticardiolipin antibodies,
  • polycythemia (hematocrit above 38%),
  • intensive use of intra- and post-transplant coagulation treatment (e.g. fresh frozen plasma).
    
• Allograft flow:
  
  • prolonged intraoperative severe hypotension or low arterial flow:
  • severe rejection causing resistance to flow by injuring microvascular network,
  • prolonged cold ischemia (>12 hours) being responsible for intimal damage or increased arterial resistance from cellular swelling,
  • portal venous overflow causing increased resistance to the arterial flow,
  • ABO incompatible liver grafting,
  • acute post-transplant pancreatitis.
    
• Cytomegalovirus (CMV) donor status (higher incidence of HAT in donor CMV positive / recipient CMV negative pair).
  

These factors have all been proven, in single center studies, to significantly influence the incidence of HAT. Most studies are however retrospective and many of them have contradicting results.
The recent experience of the Kyoto and Tokyo groups showed an extremely low incidence (<1%) of HAT in larger series of pediatric living related liver transplantation.

2.1.4. Diagnosis
The diagnosis of HAT must be aggressively searched for, especially when predisposing risk factors such as low intraoperative flow at electromagnetic flow measurement (EFM) or small donor weight are present and when new onset findings of graft dysfunction or infection appear.

Intraoperative EFM
Experiences in peripheral vascular and coronary bypass surgery have shown that intraoperative EFM is a valuable tool for direct measurement of hepatic artery and portal vein flow. Arterial flow of less than 200 mL/min in adults and of less than 60 - 50 mL/min in children indicate inadequate arterial reconstruction. Although these findings could not be confirmed in all series, EFM remains an important adjunct in the management and follow-up of these cases. Arterial compliance, measured by enhanced hepatic arterial flow under simultaneous portal vein occlusion, could be more specific.

Postoperative Doppler ultrasound
Routine surveillance with postoperative Doppler ultrasound (DUS) enables early diagnosis and treatment in most patients. DUS is highly specific and sensitive. It is of utmost importance to detect intrahepatic as well as extrahepatic flow signals. This is especially important in pediatric patients who nearly always have a bilio-enteric reconstruction. In these cases, the presence of extrahepatic signals only can be misleading as they may originate from mesenteric collaterals at the hepatico-jejunostomy. Increased diastolic flow (decreased resistive index of <0.8), systolic acceleration and high peak velocity should be followed particularly as these findings frequently precede HAT.

[点击按纽展开更多->收起->回放] Normal arterial signal at Doppler ultrasound (DUS)		[点击按纽展开更多->收起->回放] DUS arterial signal masked by very high portal vein flow
[点击按纽展开更多->收起->回放] Re-equilibration of hepatic arterial and portal vein flows shows a normal DUS arterial pattern

Angiography
Despite the high specificity of DUS examination, angiographic evaluation remains the gold standard in the diagnosis of HAT. This is even more important in late HAT; in such cases, "normal" intrahepatic flow signals may be present as a consequence of extensive arterial collateralization. DUS angiography will likely be replaced in the future by angio-magnetic nuclear imaging.

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Reduced arterial flow due to severe acute rejection at angiography, and corresponding intraoperative view of liver

2.1.5. Prevention
Perfect surgical technique and confirmation of good arterial allograft inflow, using intraoperative electromagnetic flow measurement (EFM), are the mainstays of successful hepatic artery management. Redundancy and especially kinking of the hepatic artery must be avoided; the length should be tailored to produce the shortest hepatic artery reconstruction. Very small arteries should be anastomosed using loop magnification or operating microscope.
Systemic heparinization and use of low-dose aspirin therapy have been proven to play a preventive role in HAT; however, they also bear a risk of gastrointestinal bleeding and bleeding during liver biopsy.
The Tokyo group uses an aggressive anticoagulation protocol in pediatric living related liver transplantation combining maintenance of hematocrit at around 25% and administration of low molecular weight heparin, antithrombin III, prostaglandins E 1 , fresh frozen plasma and protease inhibitor. This protocol aims at controlling a hypercoagulable state, which may potentially aggressive be induced by early allograft dysfunction.

2.1.6. Treatment
The cornerstone of therapy for HAT has for a long time been exclusively represented by re-transplantation (re-LT). Economical concerns, organ shortage and development of interventional radiology have more recently provoked a shift towards graft salvage procedures prior to re-LT.
Treatment must be based in any case on patient’s condition, clinical expression of the HAT and chronological relationship to the transplant procedure. Late HAT usually does not warrant a revascularization procedure. Delayed development of biliary strictures and intrahepatic abscesses can, as in the non-transplant setting, be treated with interventional radiological procedures, redo surgery and adapted antibiotic therapy.
On the contrary, early HAT needs an aggressive therapeutic approach. Different options are possible: urgent re-LT, urgent revascularization with or without thrombolysis, urgent or elective partial allograft resection and finally elective retransplantation.
Salvage procedures should only be considered if the recipient is hemodynamically stable, if liver function remains relatively stable, and if bacteremia can be controlled with antibiotics.
If these conditions are not fulfilled, the approach of graft hepatectomy and of re-LT remains justified. Exceptionally a two-stage procedure combining urgent total hepatectomy and later re-LT, has been advocated in order to avoid the uncontrolled septic condition or "toxic liver syndrome" caused by extensive allograft necrosis.
Urgent declotting procedures aim at revascularization in order to prevent further allograft injury. Intraoperative angiography is imperative to assess the intrahepatic circulation.

In situ thrombolysis is of particular value if intrahepatic clotting is present. Revascularization approaches have the most chances to be successful if HAT is asymptomatic and diagnosed early and if a clear-cut reason for HAT, such as intimal flap formation and anastomotic kinking, exists at reintervention. Redo of the arterial anastomosis is necessary in such cases: if the quality of the recipient's vessel is bad, one should resort to use free iliac graft interposition between abdominal infrarenal aorta and hepatic artery.
Revascularization procedures are frequently followed by recurrent (partial) thrombosis or by the development of biliary strictures as a consequence of a prolonged ischemic interval. This usually occurs within the first post-revision month. Supplementary redo surgery interventional radiology or even delayed re-LT will become necessary to definitively solve these problems. Extensive destruction of the extrahepatic biliary system can be corrected by intrahepatic cholangio-jejunostomy.
Partial allograft hepatic resection can exceptionally be indicated in selective cases presenting with sequelae of HAT such as ischemic parenchymal infarcts or biliary strictures confined to one part of the liver. Partial allograft resection is however very difficult. Removal of all septic material can offer a definitive solution in such situation; in other cases, it may convert an urgent re-LT into an elective one.
Interventional radiological drainage of localized intrahepatic abscesses represents a more elegant alternative to the more hazardous allograft resectional procedures. This treatment can be very successful, but it may last weeks to months before the necrotic areas are cured.

Early diagnosis, adapted prompt surgical and radiological treatment and management strategy (revascularization procedures vs. retransplantation) have been able to substantially modify the outlook of the patients presenting with HAT after LT. Patient survival after hepatic artery thrombosis has been raised from 36 to 86%.

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: Hepatic artery thrombosis and liver transplantation
Success of revision is related to early diagnosis and treatment, intraoperative electromagnetic flow measurement, and routine daily Doppler ultrasound.

3. References
3.1. Hepatic artery thrombosis – stenosis - diagnosis

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3.2. Arterial reconstruction technique

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Shaw BW, Jr., Iwatsuki S, Starzl TE. Alternative methods of arterialization of the hepatic graft. Surg Gynecol Obstet 1984;159:490-3.

Starzl TE, Iwatsuki S, Shaw BW, Jr. A growth factor in fine vascular anastomoses. Surg Gynecol Obstet 1984;159:164-5.

Stewart MT, Millikan WJ, Jr., Henderson JM, Galloway JR, Dodson TF. Proximal abdominal graft for arterialization during hepatic transplantation. Surg Gynecol Obstet 1989;169:261-2.
3.3. Hepatic artery thrombosis

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Hashikura Y, Kawasaki S, Okumura N, Ishikawa S, Matsunami H, Ikegami T, et al. Prevention of hepatic artery thrombosis in pediatric liver transplantation. Transplantation 1995;60:1109-12.

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Houssin D, Fratacci M, Dupuy P, Vigouroux C, Gatecel C, Payen D, et al. One week of monitoring of portal and hepatic arterial blood flow after liver transplantation using implantable pulsed Doppler microprobes. Transplant Proc 1989;21:2277-8.

Huang CJ, Pitt HA, Lipsett PA, Osterman FA, Jr., Lillemoe KD, Cameron JL, et al. Pyogenic hepatic abscess. Changing trends over 42 years. Ann Surg 1996;223:600-7; discussion 607-9.

Ikegami T, Kawasaki S, Hashikura Y, Miwa S, Kubota T, Mita A, et al. An alternative method of arterial reconstruction after hepatic arterial thrombosis following living-related liver transplantation. Transplantation 2000;69:1953-5.

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Langnas AN, Marujo W, Stratta RJ, Wood RP, Li SJ, Shaw BW. Hepatic allograft rescue following arterial thrombosis. Role of urgent revascularization. Transplantation 1991;51:86-90.

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Sheiner PA, Varma CV, Guarrera JV, Cooper J, Garatti M, Emre S, et al. Selective revascularization of hepatic artery thromboses after liver transplantation improves patient and graft survival. Transplantation 1997;64:1295-9.

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Zajko AB, Bron KM, Starzl TE, Van Thiel DH, Gartner JC, Iwatsuki S, et al. Angiography of liver transplantation patients. Radiology 1985;157:305-11.
3.4. Partial hepatic artery thrombosis

Lurie AS. The significance of the variant left accessory hepatic artery in surgery for proximal gastric cancer. Arch Surg 1987;122:725-8.

Mays ET, 2nd, Mays ET. Are hepatic arteries end-arteries? J Anat 1983;137:637-44.

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