Liver transplantation complications: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
No edit summary
 
(4 intermediate revisions by the same user not shown)
Line 4: Line 4:
{{Liver transplantation}}
{{Liver transplantation}}
==Overview==
==Overview==
Complications of liver transplantation include [[vascular]], [[biliary]], and [[Immunosuppressive therapy|immunosuppression drugs]] complications. [[Hepatic artery]] complications include [[thrombosis]], [[stenosis]], and [[pseudoaneurysm]]. [[Inferior vena cava|IVC]] complications include [[thrombosis]] and [[stenosis]], usually at the site of [[surgical anastomosis]]. [[Bile duct|Biliary]] complications include [[stenosis]], [[fistula]], [[obstruction]], [[Cholelithiasis|stone]] formation, dysfunction of the [[Sphincter of Oddi dysfunction|Oddi sphincter]], and recurrent biliary disease. Complications of [[immunosupression]] include [[Infection|infections]], [[metabolic syndrome]], [[hypertension]], [[diabetes mellitus]], [[obesity]], [[dyslipidemia]], [[coronary heart disease]], acute and [[Chronic renal failure|chronic renal disease]], metabolic bone disease, and [[malignancy]].


== Post-surgical complications ==
== Post-surgical complications ==
Line 10: Line 11:


==== Hepatic Artery ====
==== Hepatic Artery ====
Hepatic artery complications include thrombosis, stenosis, and pseudoaneurysm.  
* Hepatic artery complications include [[thrombosis]], [[stenosis]], and [[pseudoaneurysm]].  
 
* A normal hepatic artery waveform obtained at the [[porta hepatis]] does not exclude a [[hepatic artery]] obstruction.<ref name="pmid16967253">{{cite journal| author=Tamsel S, Demirpolat G, Killi R, Aydin U, Kilic M, Zeytunlu M et al.| title=Vascular complications after liver transplantation: evaluation with Doppler US. | journal=Abdom Imaging | year= 2007 | volume= 32 | issue= 3 | pages= 339-47 | pmid=16967253 | doi=10.1007/s00261-006-9041-z | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16967253  }}</ref>
a normal hepatic artery waveform obtained at the porta hepatis does not exclude a hepatic artery obstruction (15).  
 
In the early postoperative period (<72 hours after transplantation), increased hepatic artery resistance (resistive index of >0.8) is a frequent finding, but resistance ordinarily returns to a normal level within a few days. (18).


==== Thrombosis ====
==== Thrombosis ====
* The estimated incidence of hepatic artery thrombosis among liver transplant recipients is 4%–12% in adults and 42% in children. (12,19).  
* The incidence of hepatic artery thrombosis is 4%–12% in adults and 42% in children.<ref name="pmid23622659">{{cite journal| author=Väli T, Tein A, Tiganik V, Ulst K| title=Vascular complications after orthotopic liver transplantation in Estonia. | journal=Transplant Proc | year= 2013 | volume= 45 | issue= 3 | pages= 1201-3 | pmid=23622659 | doi=10.1016/j.transproceed.2012.10.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23622659  }}</ref>
* it may lead to fulminant hepatic necrosis. the mortality rate approaches 30% (3).
* The [[mortality rate]]<nowiki/>s are 30% due to [[fulminant hepatic necrosis]].<ref name="pmid11866218">{{cite journal| author=García-Criado A, Gilabert R, Bargalló X, Brú C| title=Radiology in liver transplantation. | journal=Semin Ultrasound CT MR | year= 2002 | volume= 23 | issue= 1 | pages= 114-29 | pmid=11866218 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11866218  }}</ref>
* In addition, in liver grafts, biliary ducts are supplied exclusively by small branches of the hepatic artery; therefore, arterial thrombosis may lead to biliary ischemia and necrosis (4,8,15).
* [[Arterial thrombosis]] may lead to [[biliary]] necrosis.
* early intervention may allow graft salvage. However, most patients ultimately require retransplantation. (14)
* Most cases require retransplantation.<ref name="pmid11259700">{{cite journal| author=Glockner JF| title=Three-dimensional gadolinium-enhanced MR angiography: applications for abdominal imaging. | journal=Radiographics | year= 2001 | volume= 21 | issue= 2 | pages= 357-70 | pmid=11259700 | doi=10.1148/radiographics.21.2.g01mr14357 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11259700  }}</ref>
* Risk factors for hepatic artery thrombosis include a significant difference in hepatic artery caliber between the donor and the recipient. (12,14,19,20).
* [[Gadolinium]]-enhanced [[Magnetic resonance imaging|MR]] imaging is an accurate and noninvasive method for evaluating the hepatic vessels.
* A US-based diagnosis of hepatic artery thrombosis is established in the absence of flow in the proper hepatic and intrahepatic artery at color and pulsed Doppler imaging (Fig 3).
* Gadolinium-enhanced MR imaging with three-dimensional spoiled gradient-echo sequences is another accurate and noninvasive method for evaluating the hepatic vessels (2,5,13,25).


==== Stenosis ====
==== Stenosis ====
* Hepatic artery stenosis has been reported to occur in 5%–11% of liver transplant recipients (3,4,12).  
* [[Hepatic artery]] [[stenosis]] incidence rates are 5%–11% of liver transplant recipients.  
* This complication usually occurs at the site of anastomosis within 3 months after transplantation (3).
* This [[Complication (medicine)|complication]] usually occurs at the site of [[anastomosis]] within 3 months after transplantation.
* Causes of hepatic artery stenosis may include clamp injury, intimal trauma from a perfusion catheter, or disruption of the vasa vasorum with resultant ischemia of the arterial ends (8).
* Causes of hepatic artery [[stenosis]] may include injury from a perfusion [[catheter]], or disruption of the [[vasa vasorum]] with resultant [[ischemia]] of the arterial ends.<ref name="pmid8058930">{{cite journal| author=Dodd GD, Memel DS, Zajko AB, Baron RL, Santaguida LA| title=Hepatic artery stenosis and thrombosis in transplant recipients: Doppler diagnosis with resistive index and systolic acceleration time. | journal=Radiology | year= 1994 | volume= 192 | issue= 3 | pages= 657-61 | pmid=8058930 | doi=10.1148/radiology.192.3.8058930 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8058930  }}</ref>
* Duplex Doppler US is the method of choice for postoperative screening of liver transplant recipients because it is capable of depicting any focal increase (of more than two to three times) in peak systolic velocity at the site of stenosis and any poststenotic turbulent flow (17).  
* [[Medical ultrasonography|Doppler US]] is the method of choice for postoperative screening of liver transplant recipients because it is capable of depicting any focal increase in peak systolic velocity at the site of stenosis and any poststenotic [[turbulent flow]].  
* Both at contrast-enhanced CT and at MR angiography, this arterial lesion appears enhanced (4,14).
* Both at [[Contrast enhanced CT|contrast-enhanced CT]] and at [[Magnetic resonance angiography|MR angiography]], this arterial lesion appears enhanced.


==== Portal Vein ====
==== Portal Vein ====
* Portal vein thrombosis occurs in about 1%–2% of cases (12,19).  
* [[Portal vein thrombosis]] occurs in about 1%–2% of cases.<ref name="pmid115538182">{{cite journal| author=Quiroga S, Sebastià MC, Margarit C, Castells L, Boyé R, Alvarez-Castells A| title=Complications of orthotopic liver transplantation: spectrum of findings with helical CT. | journal=Radiographics | year= 2001 | volume= 21 | issue= 5 | pages= 1085-102 | pmid=11553818 | doi=10.1148/radiographics.21.5.g01se061085 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11553818  }}</ref>
* It most commonly results from technical problems (vessel misalignment, differences in the caliber of the anastomosed vessels, or stretching of the portal vein at the anastomotic site), previous portal vein surgery or previous thrombosis, increased downstream resistance due to a supra-hepatic stricture of the inferior vena cava (IVC), decreased portal inflow, and hypercoagulable states (3,4).
* It most commonly results from technical problems (vessel misalignment, differences in the caliber of the anastomosed vessels, or stretching of the portal vein at the anastomotic site), previous portal vein surgery or previous thrombosis, increased downstream resistance due to a supra-hepatic stricture of the inferior vena cava (IVC), decreased portal inflow, and hypercoagulable states.
* Portal vein stenosis has a reported incidence of 1% after liver transplantation (12).  
* Portal vein [[stenosis]] has a reported incidence of 1% after liver transplantation.  
* The treatment in symptomatic cases is thrombolysis or surgery (thrombectomy, venous graft) (4).
* The treatment in symptomatic cases is [[thrombolysis]] or surgery ([[thrombectomy]], venous graft)
* CT and MR angiography provide excellent depiction of filling defects and focal narrowing of the portal vein (Fig 11) (3,13). Rarely, transhepatic or transjugular portography may be necessary to achieve a definitive diagnosis (27). IVC and Hepatic Vein
* [[CT-scans|CT]] and [[MR angiography]] provide excellent depiction of filling defects and focal narrowing of the portal vein.
* Transhepatic or transjugular portography may be necessary to achieve a definitive diagnosis.<ref name="pmid9225389">{{cite journal| author=Pieters PC, Miller WJ, DeMeo JH| title=Evaluation of the portal venous system: complementary roles of invasive and noninvasive imaging strategies. | journal=Radiographics | year= 1997 | volume= 17 | issue= 4 | pages= 879-95 | pmid=9225389 | doi=10.1148/radiographics.17.4.9225389 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9225389  }}</ref>


==== Inferior Vena Cava ====
==== Inferior Vena Cava (IVC) ====
* IVC complications include thrombosis and stenosis, usually at the site of surgical anastomosis
* [[Inferior vena cava|IVC]] complications include [[thrombosis]] and [[stenosis]], usually at the site of [[surgical anastomosis]].<ref name="pmid10507483">{{cite journal| author=Navarro F, Le Moine MC, Fabre JM, Belghiti J, Cherqui D, Adam R et al.| title=Specific vascular complications of orthotopic liver transplantation with preservation of the retrohepatic vena cava: review of 1361 cases. | journal=Transplantation | year= 1999 | volume= 68 | issue= 5 | pages= 646-50 | pmid=10507483 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10507483  }}</ref>
* The “piggyback” anastomosis (with preservation of the recipient vena cava and cavocaval anastomosis) has gained wide acceptance internationally and is the preferred technique for orthotopic liver transplantation at many institutions (28).  
* The anastomosis gained wide acceptance internationally and is the preferred technique for orthotopic liver transplantation at many institutions.  
* However, it is especially vulnerable to two types of complications: (a) hemorrhage due to hepatic injury during surgery or due to cavocaval dehiscence (3% of cases) and (b) Budd-Chiari syndrome (0.3%–1.5% of cases) due to inadequate venous drainage (29). An obstruction of hepatic venous outflow may be treated with placement of a balloon-expandable stent (28).
* However, it is especially vulnerable to two types of complications:  
* Cross-sectional modalities such as CT and MR imaging are commonly used to confirm suspicions aroused by Doppler US findings or to exclude a clinical hypothesis when US results are normal or inconclusive (Fig 13c–13e). In addition to stricture or thrombosis, CT and MR images may show additional diagnostic features, such as a mosaic pattern of perfusion (characteristic of Budd-Chiari syndrome) (Fig 14c, 14d) (3).
* [[Hemorrhage]] due to hepatic injury during surgery
* [[Budd-Chiari syndrome]] due to inadequate venous drainage<ref name="pmid15955856">{{cite journal| author=Wang SL, Sze DY, Busque S, Razavi MK, Kee ST, Frisoli JK et al.| title=Treatment of hepatic venous outflow obstruction after piggyback liver transplantation. | journal=Radiology | year= 2005 | volume= 236 | issue= 1 | pages= 352-9 | pmid=15955856 | doi=10.1148/radiol.2361040327 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15955856  }}</ref>
* An obstruction of hepatic venous outflow may be treated with placement of a balloon-expandable stent.
* Cross-sectional modalities such as [[CT]] and [[Magnetic resonance imaging|MR]] imaging are commonly used to confirm suspicions aroused by doppler [[Ultrasound|US]] findings.  


=== Biliary Disorders ===
=== Biliary Disorders ===
* Biliary complications include stenosis, fistula, obstruction, stone formation, dysfunction of the Oddi sphincter, and recurrent biliary disease (7).
* [[Bile duct|Biliary]] complications include [[stenosis]], [[fistula]], [[obstruction]], [[Cholelithiasis|stone]] formation, dysfunction of the [[Sphincter of Oddi dysfunction|Oddi sphincter]], and recurrent biliary disease.<ref name="pmid14990819">{{cite journal| author=Ward J, Sheridan MB, Guthrie JA, Davies MH, Millson CE, Lodge JP et al.| title=Bile duct strictures after hepatobiliary surgery: assessment with MR cholangiography. | journal=Radiology | year= 2004 | volume= 231 | issue= 1 | pages= 101-8 | pmid=14990819 | doi=10.1148/radiol.2311030017 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14990819  }}</ref>
* MR cholangiography is the best noninvasive technique for evaluation of the biliary tree (1,27).  
* MR cholangiography is the best noninvasive technique for evaluation of the biliary tree. It does not provide a means of therapeutic intervention, it can be used for percutaneous, [[Endoscopy|endoscopic]], and surgical treatments.  
* Multiplanar MR imaging enables accurate analysis of the surgically altered biliary anatomy. Although it does not provide a means of therapeutic intervention, it can be used to plan percutaneous, endoscopic, and surgical treatments (1). Despite good sensitivity for the detection of strictures, MR cholangiography tends to lead to their overestimation (31).
* [[Endoscopic retrograde cholangiopancreatography]] and [[percutaneous transhepatic cholangiography]] provide high-quality images of the biliary tree and allow therapeutic intervention.  
* Endoscopic retrograde cholangiopancreatography and percutaneous transhepatic cholangiography provide high-quality images of the biliary tree and allow therapeutic intervention. However, the modalities are invasive and are associated with complications, which occur in 3.4% of percutaneous transhepatic cholangiographic examinations and in 5% of endoscopic retrograde cholangiopancreatographic examinations (1,27).


==== Obstruction and Stenosis ====
==== Obstruction and Stenosis ====
* Obstruction is the most common biliary complication both in adults and in pediatric patients and is frequently caused by stenosis at the anastomotic site (1). Anastomotic strictures usually result from fibrotic proliferation with narrowing of the biliary lumen (Fig 15); less frequently, they are due to ischemia caused by hepatic artery thrombosis or stenosis (1). The possible causes of nonanastomotic strictures include pretransplantation biliary diseases such as primary sclerosing cholangitis, biliary ischemia, and infection.
* [[Obstruction]] is the most common biliary complication both in adults and in pediatric patients and is frequently caused by stenosis at the anastomotic site.<ref name="pmid10352596">{{cite journal| author=Fulcher AS, Turner MA| title=Orthotopic liver transplantation: evaluation with MR cholangiography. | journal=Radiology | year= 1999 | volume= 211 | issue= 3 | pages= 715-22 | pmid=10352596 | doi=10.1148/radiology.211.3.r99jn17715 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10352596  }}</ref>
* When biliary obstruction is believed to be present in a liver graft, it is of paramount importance that imaging findings be correlated with clinical and laboratory findings. Mild dilatation of the biliary tree may be observed on images in the absence of an actual mechanical obstruction (1). On the other hand, clinical and laboratory evidence of high-grade obstruction may be observed without visible dilatation of the biliary tree (3). Some patients with clinical and biochemical evidence of biliary obstruction may have dilatation of both the donor and the recipient bile ducts. Diffuse ductal dilatation may result from papillary dyskinesia due to devascularization or denervation of the papilla of Vater during transplantation (1).
* Anastomotic [[strictures]] usually result from fibrotic proliferation with narrowing of the biliary lumen less frequently, they are due to [[ischemia]] caused by [[hepatic artery]] [[thrombosis]] or [[Stenosis|stenosis.]]
* The possible causes of nonanastomotic strictures include pretransplantation biliary diseases such as [[primary sclerosing cholangitis]], biliary [[ischemia]], and [[infection]].
* Some patients with clinical and [[Biochemical|biochemical evidence]] of [[biliary obstruction]] may have dilatation of both the donor and the recipient bile ducts.  
* Diffuse ductal dilatation may result from papillary [[dyskinesia]] due to devascularization or denervation of the papilla of Vater during transplantation.


==== Bile Leak ====
==== Bile Leak ====
* The approximate incidence of bile leaks in liver transplant recipients is 5%. Bile leaks usually occur in the early posttransplantation period, and more than 70% occur within the 1st postoperative month (4). Leaks occur most often at the T-tube site and rarely at the site of an anastomosis (3). Bile may leak freely into the peritoneal cavity or may form a perihepatic collection (Fig 16). Treatment includes stent placement and drainage of collections (8).
* The [[incidence]] of bile leaks in liver transplant recipients is 5%.  
* Bile leaks usually occur in more than 70% occur within the 1st postoperative month.
* Leaks occur most often at the T-tube site.
* [[Bile]] may leak freely into the peritoneal cavity or may form a perihepatic collection.
* Treatment includes stent placement and drainage of collections.


==== Ductal Ischemia ====
==== Ductal Ischemia ====
* Bile duct ischemia is usually a consequence of stenosis or thrombosis of the hepatic artery; the bile ducts are entirely dependent on the hepatic artery for their blood supply (14,32). The results of ductal ischemia are necrosis and its associated complications: bile leak (fistula), ductal scarring with fibrosis (stenosis), and bile collection  
* [[Bile duct]] [[ischemia]] is usually a consequence of [[stenosis]] or [[thrombosis]] of the [[hepatic artery]]; the [[bile ducts]] are entirely dependent on the [[hepatic artery]] for their blood supply.<ref name="pmid7572493">{{cite journal| author=Orons PD, Sheng R, Zajko AB| title=Hepatic artery stenosis in liver transplant recipients: prevalence and cholangiographic appearance of associated biliary complications. | journal=AJR Am J Roentgenol | year= 1995 | volume= 165 | issue= 5 | pages= 1145-9 | pmid=7572493 | doi=10.2214/ajr.165.5.7572493 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7572493  }}</ref>
* This leads to [[necrosis]], bile leak, [[fibrosis]], and bile collection.
* A ductal stenosis may be treated with balloon dilation, which frequently is used in drainage procedures.  
* A ductal stenosis may be treated with balloon dilation, which frequently is used in drainage procedures.  
* However, in most cases, retransplantation ultimately is necessary (3).  
* However, in most cases, retransplantation ultimately is necessary.  


==== Fluid Collections ====
==== Fluid Collections ====
* Seromas and hematomas are commonly observed near areas of vascular anastomosis (the hepatic hilum, the IVC) and biliary anastomosis, as well as in the perihepatic spaces. Such collections usually are found during the first days after transplantation and disappear within a few weeks (Fig 18). Rarely, they are large enough to compress the portal vein or the IVC.  
* [[Seroma|Seromas]] and [[Hematoma|hematomas]] are commonly observed near areas of vascular [[anastomosis]] and biliary anastomosis.
* Pleural fluid, especially in the right side, also is a common finding. There is rarely a need for intervention if there is no ventilatory compromise (3).
* Pleural fluid also is a common finding.
* Although US is highly sensitive for the detection of fluid collections, it is not specific. A hematoma or purulent abscess may resemble a particulate ascites on US images.
* [[Ultrasound|US]] is highly sensitive for the detection of fluid collections, it is not specific.
* However, in most cases, collections of bile, lymph, blood, and pus all have the same appearance of a simple fluid collection (8).
* [[CT-scans|CT]] and [[Magnetic resonance imaging|MR]] imaging are more useful for differentiating [[Hematoma|hematomas]] from [[Seroma|seromas]] because [[blood]] has higher attenuation at [[Computed tomography|CT]] than do other fluids.
* As expected, CT and MR imaging (especially the latter) are more useful for differentiating hematomas from seromas and bilomas because blood has higher attenuation at CT than do other fluids (3) and has a characteristic signal intensity at MR imaging. Nevertheless, it is difficult to distinguish a bile leak from a periportal seroma at MR imaging (33).  
* The other role of imaging is to guide interventional diagnostic or therapeutic procedures.  
* In some cases, the main role of imaging is to pinpoint the amount and location of such collections and, when possible, to guide interventional diagnostic or therapeutic procedures.
'''COMPLICATIONS OF IMMUNOSUPPRESSION'''


==== '''Complications of immunosupression''' ====
'''Infections'''
'''Infections'''
* The leading cause of mortality following liver transplantation is infection.<ref name="pmid9455510">{{cite journal| author=Chang FY, Singh N, Gayowski T, Wagener MM, Marino IR| title=Fever in liver transplant recipients: changing spectrum of etiologic agents. | journal=Clin Infect Dis | year= 1998 | volume= 26 | issue= 1 | pages= 59-65 | pmid=9455510 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9455510  }}</ref>
* The leading cause of [[Mortality rate|mortality]] following liver transplantation is [[infection]].<ref name="pmid9455510">{{cite journal| author=Chang FY, Singh N, Gayowski T, Wagener MM, Marino IR| title=Fever in liver transplant recipients: changing spectrum of etiologic agents. | journal=Clin Infect Dis | year= 1998 | volume= 26 | issue= 1 | pages= 59-65 | pmid=9455510 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9455510  }}</ref>
* Serious infections occur most frequently within the first three months post-transplantation, which is the time of greatest immunosuppression.
* Serious infections occur most frequently within the first three months post-transplantation.
'''Metabolic syndrome'''
'''Metabolic syndrome'''
* The metabolic syndrome is common among patients who have undergone liver transplantation. It is defined by a combination of hypertension, insulin resistance/diabetes, dyslipidemia, and obesity.<ref name="pmid25880971">{{cite journal| author=Fussner LA, Heimbach JK, Fan C, Dierkhising R, Coss E, Leise MD et al.| title=Cardiovascular disease after liver transplantation: When, What, and Who Is at Risk. | journal=Liver Transpl | year= 2015 | volume= 21 | issue= 7 | pages= 889-96 | pmid=25880971 | doi=10.1002/lt.24137 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25880971  }}</ref>
* The [[metabolic syndrome]] is common among patients who have undergone liver transplantation.  
* Liver transplant recipients may meet criteria for the metabolic syndrome prior to transplantation, in which case immunosuppressive medications can exacerbate the problem. In addition, many patients will develop the metabolic syndrome de novo.<ref name="pmid21254340">{{cite journal| author=Laish I, Braun M, Mor E, Sulkes J, Harif Y, Ben Ari Z| title=Metabolic syndrome in liver transplant recipients: prevalence, risk factors, and association with cardiovascular events. | journal=Liver Transpl | year= 2011 | volume= 17 | issue= 1 | pages= 15-22 | pmid=21254340 | doi=10.1002/lt.22198 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21254340  }}</ref>
* It is defined by a combination of [[hypertension]], [[insulin resistance]], [[dyslipidemia]], and [[obesity]].<ref name="pmid25880971">{{cite journal| author=Fussner LA, Heimbach JK, Fan C, Dierkhising R, Coss E, Leise MD et al.| title=Cardiovascular disease after liver transplantation: When, What, and Who Is at Risk. | journal=Liver Transpl | year= 2015 | volume= 21 | issue= 7 | pages= 889-96 | pmid=25880971 | doi=10.1002/lt.24137 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25880971  }}</ref>
* A study of 252 liver transplant patients found that 52 percent had metabolic syndrome following transplantation, compared with only 5 percent prior to transplantation.
* Liver transplant recipients may meet criteria for the [[metabolic syndrome]] prior to transplantation, in which case [[Immunosuppressive therapy|immunosuppressive medications]] can exacerbate the problem.  
* A second study with 455 liver transplant recipients found that the rate of obesity increased from 24 percent four months after transplantation to 41 percent three years after transplantation.
* In addition, many patients will develop the metabolic syndrome de novo.<ref name="pmid21254340">{{cite journal| author=Laish I, Braun M, Mor E, Sulkes J, Harif Y, Ben Ari Z| title=Metabolic syndrome in liver transplant recipients: prevalence, risk factors, and association with cardiovascular events. | journal=Liver Transpl | year= 2011 | volume= 17 | issue= 1 | pages= 15-22 | pmid=21254340 | doi=10.1002/lt.22198 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21254340  }}</ref>
* Fifty-two percent had [[metabolic syndrome]] following transplantation, compared with only 5 percent prior to transplantation.
* The rate of [[obesity]] increased from 24 percent four months after transplantation to 41 percent three years after transplantation.
Immunosuppressant use is associated with all aspects of the metabolic syndrome:
Immunosuppressant use is associated with all aspects of the metabolic syndrome:
* Hypertension: Glucocorticoids, cyclosporine >tacrolimus
* [[Hypertension]]: [[Glucocorticoids]], [[cyclosporine]], [[tacrolimus]]
* Diabetes mellitus: Glucocorticoids, tacrolimus >cyclosporine
* [[Diabetes mellitus]]: [[Glucocorticoids]], [[tacrolimus]], [[cyclosporine]]
* Obesity: Glucocorticoids, cyclosporine
* [[Obesity]]: [[Glucocorticoids]], [[cyclosporine]]
* Dyslipidemia: Glucocorticoids, cyclosporine >tacrolimus, sirolimus
* [[Dyslipidemia]]: [[Glucocorticoids]], [[cyclosporine]]. [[tacrolimus]], [[sirolimus]]
'''Hypertension'''
'''Hypertension'''
* Approximately 65 to 70 percent of liver transplant recipients develop hypertension following transplantation.<ref name="pmid7544983">{{cite journal| author=Taler SJ, Textor SC, Canzanello VJ, Wilson DJ, Wiesner RH, Krom RA| title=Loss of nocturnal blood pressure fall after liver transplantation during immunosuppressive therapy. | journal=Am J Hypertens | year= 1995 | volume= 8 | issue= 6 | pages= 598-605 | pmid=7544983 | doi=10.1016/0895-7061(95)00077-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7544983  }}</ref>  
* Approximately 65 to 70 percent of liver transplant recipients develop [[hypertension]] following transplantation.<ref name="pmid7544983">{{cite journal| author=Taler SJ, Textor SC, Canzanello VJ, Wilson DJ, Wiesner RH, Krom RA| title=Loss of nocturnal blood pressure fall after liver transplantation during immunosuppressive therapy. | journal=Am J Hypertens | year= 1995 | volume= 8 | issue= 6 | pages= 598-605 | pmid=7544983 | doi=10.1016/0895-7061(95)00077-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7544983  }}</ref>  
* In addition, some patients lose the normal circadian blood pressure patterns and develop nocturnal hypertension. Because hypertension is common post-transplantation, we suggest that for the first six months following transplantation, the patient's blood pressure be assessed at home with self-monitoring every week and by a
* Patient's [[blood pressure]] be assessed at home with self-monitoring every week for six months after the surgery.
* The cause of hypertension is multifactorial but is mostly related to the use of calcineurin inhibitors (CNIs; eg, cyclosporine or tacrolimus) and glucocorticoids.<ref name="pmid9346597">{{cite journal| author=Textor SC, Canzanello VJ, Taler SJ, Schwartz L, Augustine J| title=Hypertension after liver transplantation. | journal=Liver Transpl Surg | year= 1995 | volume= 1 | issue= 5 Suppl 1 | pages= 20-8 | pmid=9346597 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9346597  }}</ref>  
* The cause of hypertension is multifactorial but is mostly related to the use of [[Calcineurin inhibitor|calcineurin inhibitors]] and [[glucocorticoids]].<ref name="pmid9346597">{{cite journal| author=Textor SC, Canzanello VJ, Taler SJ, Schwartz L, Augustine J| title=Hypertension after liver transplantation. | journal=Liver Transpl Surg | year= 1995 | volume= 1 | issue= 5 Suppl 1 | pages= 20-8 | pmid=9346597 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9346597  }}</ref><ref name="pmid21251543">{{cite journal| author=Mangray M, Vella JP| title=Hypertension after kidney transplant. | journal=Am J Kidney Dis | year= 2011 | volume= 57 | issue= 2 | pages= 331-41 | pmid=21251543 | doi=10.1053/j.ajkd.2010.10.048 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21251543  }}</ref>  
* CNIs act by increasing both systemic vascular resistance and renal vascular resistance (primarily affecting the afferent arterioles).<ref name="pmid21251543">{{cite journal| author=Mangray M, Vella JP| title=Hypertension after kidney transplant. | journal=Am J Kidney Dis | year= 2011 | volume= 57 | issue= 2 | pages= 331-41 | pmid=21251543 | doi=10.1053/j.ajkd.2010.10.048 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21251543  }}</ref>  
'''Diabetes mellitus'''
'''Diabetes mellitus'''
* Glucocorticoids, cyclosporine, tacrolimus, and weight gain predispose to the development of diabetes following liver transplantation.  
* [[Glucocorticoids]], [[cyclosporine]], [[tacrolimus]], and [[weight gain]] predispose to the development of diabetes following liver transplantation.  
* The risk also appears to be increased in patients transplanted for hepatitis C virus.<ref name="pmid25413020">{{cite journal| author=Younossi Z, Stepanova M, Saab S, Trimble G, Mishra A, Henry L| title=The association of hepatitis C virus infection and post-liver transplant diabetes: data from 17 000 HCV-infected transplant recipients. | journal=Aliment Pharmacol Ther | year= 2015 | volume= 41 | issue= 2 | pages= 209-17 | pmid=25413020 | doi=10.1111/apt.13027 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25413020  }}</ref>
* The risk also appears to be increased in patients transplanted for [[hepatitis C virus]].<ref name="pmid25413020">{{cite journal| author=Younossi Z, Stepanova M, Saab S, Trimble G, Mishra A, Henry L| title=The association of hepatitis C virus infection and post-liver transplant diabetes: data from 17 000 HCV-infected transplant recipients. | journal=Aliment Pharmacol Ther | year= 2015 | volume= 41 | issue= 2 | pages= 209-17 | pmid=25413020 | doi=10.1111/apt.13027 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25413020  }}</ref>
* To screen for diabetes we obtain fasting plasma glucose levels or hemoglobin A1C every six months. We also obtain annual eye examinations to look for cataracts or diabetic changes.
* [[Fasting plasma glucose]] levels or hemoglobin A1C are sceened every six months and annual eye examinations to look for cataracts or diabetic changes.
'''Obesity'''
'''Obesity'''
* Patients with end-stage liver disease frequently have a compromised nutritional status. Despite this, over one-third of patients are obese.<ref name="pmid18975273">{{cite journal| author=Bianchi G, Marchesini G, Marzocchi R, Pinna AD, Zoli M| title=Metabolic syndrome in liver transplantation: relation to etiology and immunosuppression. | journal=Liver Transpl | year= 2008 | volume= 14 | issue= 11 | pages= 1648-54 | pmid=18975273 | doi=10.1002/lt.21588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18975273  }}</ref>  
* Over one-third of patients after liver transplantation are obese.<ref name="pmid18975273">{{cite journal| author=Bianchi G, Marchesini G, Marzocchi R, Pinna AD, Zoli M| title=Metabolic syndrome in liver transplantation: relation to etiology and immunosuppression. | journal=Liver Transpl | year= 2008 | volume= 14 | issue= 11 | pages= 1648-54 | pmid=18975273 | doi=10.1002/lt.21588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18975273  }}</ref>  
* Following transplantation, improved health and treatment with glucocorticoids or cyclosporinepredispose to weight gain. Approximately one-third of patients who are normal weight at the time of transplantation will become obese following transplantation.<ref name="pmid9377752">{{cite journal| author=Canzanello VJ, Schwartz L, Taler SJ, Textor SC, Wiesner RH, Porayko MK et al.| title=Evolution of cardiovascular risk after liver transplantation: a comparison of cyclosporine A and tacrolimus (FK506). | journal=Liver Transpl Surg | year= 1997 | volume= 3 | issue= 1 | pages= 1-9 | pmid=9377752 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9377752  }}</ref>  
* Approximately one-third of patients who are normal weight at the time of transplantation will become obese following transplantation.<ref name="pmid9377752">{{cite journal| author=Canzanello VJ, Schwartz L, Taler SJ, Textor SC, Wiesner RH, Porayko MK et al.| title=Evolution of cardiovascular risk after liver transplantation: a comparison of cyclosporine A and tacrolimus (FK506). | journal=Liver Transpl Surg | year= 1997 | volume= 3 | issue= 1 | pages= 1-9 | pmid=9377752 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9377752  }}</ref>  
* Body weight tends to increase during the first two years after transplantation and then stabilizes. As an example, in one series of 774 patients, mean body mass index increased from 24.8 kg/m<sup>2</sup> at baseline to 27.0 kg/m<sup>2</sup> at year 1, to 28.1 kg/m<sup>2</sup> at year 2; there was very little change with subsequent observations.<ref name="pmid9649642">{{cite journal| author=Everhart JE, Lombardero M, Lake JR, Wiesner RH, Zetterman RK, Hoofnagle JH| title=Weight change and obesity after liver transplantation: incidence and risk factors. | journal=Liver Transpl Surg | year= 1998 | volume= 4 | issue= 4 | pages= 285-96 | pmid=9649642 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9649642  }}</ref>
* Body weight tends to increase during the first two years after transplantation and then stabilizes.<ref name="pmid9649642">{{cite journal| author=Everhart JE, Lombardero M, Lake JR, Wiesner RH, Zetterman RK, Hoofnagle JH| title=Weight change and obesity after liver transplantation: incidence and risk factors. | journal=Liver Transpl Surg | year= 1998 | volume= 4 | issue= 4 | pages= 285-96 | pmid=9649642 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9649642  }}</ref>
'''Dyslipidemia'''
'''Dyslipidemia'''
* Dyslipidemia is common after liver transplantation, and patients should have a fasting lipid profile obtained annually.<ref name="pmid9346772">{{cite journal| author=Gisbert C, Prieto M, Berenguer M, Bretó M, Carrasco D, de Juan M et al.| title=Hyperlipidemia in liver transplant recipients: prevalence and risk factors. | journal=Liver Transpl Surg | year= 1997 | volume= 3 | issue= 4 | pages= 416-22 | pmid=9346772 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9346772 }}</ref>
* [[Dyslipidemia]] is common after liver transplantation.
* Hypercholesterolemia develops in 16 to 43 percent of patients and hypertriglyceridemia in 40 to 47 percent; reduced serum HDL-cholesterol is also common.
* [[Hypertriglyceridemia laboratory tests|Hypertriglyceridemia]] usually develops within the first month post-transplantation and then remains stable throughout the first year.
* Hypertriglyceridemia usually develops within the first month post-transplantation and then remains stable throughout the first year. By comparison, serum cholesterol increases gradually and plateaus at six months.
* [[Cholesterol|Serum cholesterol]] increases gradually and plateaus at six months.<ref name="pmid17606214">{{cite journal| author=Liu LU, Schiano TD| title=Long-term care of the liver transplant recipient. | journal=Clin Liver Dis | year= 2007 | volume= 11 | issue= 2 | pages= 397-416 | pmid=17606214 | doi=10.1016/j.cld.2007.04.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17606214 }}</ref>
* Patients with elevated pretransplantation cholesterol levels are most likely to develop hypercholesterolemia following transplantation.<ref name="pmid17606214">{{cite journal| author=Liu LU, Schiano TD| title=Long-term care of the liver transplant recipient. | journal=Clin Liver Dis | year= 2007 | volume= 11 | issue= 2 | pages= 397-416 | pmid=17606214 | doi=10.1016/j.cld.2007.04.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17606214 }}</ref>
* Patients should have a fasting [[lipid profile]] obtained annually.<ref name="pmid9346772">{{cite journal| author=Gisbert C, Prieto M, Berenguer M, Bretó M, Carrasco D, de Juan M et al.| title=Hyperlipidemia in liver transplant recipients: prevalence and risk factors. | journal=Liver Transpl Surg | year= 1997 | volume= 3 | issue= 4 | pages= 416-22 | pmid=9346772 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9346772 }}</ref>
'''Cardiovascular risk'''
'''Cardiovascular risk'''
* Because of the high rates of hypertension, diabetes, obesity, and dyslipidemia following liver transplantation, it is not surprising that coronary heart disease is also common. A meta-analysis that included 4792 patients following liver transplantation with 28,783 person-years of follow-up found that the 10-year risk of cardiovascular events was 14 percent and was particularly high among those with the metabolic syndrome.<ref name="pmid22140067">{{cite journal| author=Albeldawi M, Aggarwal A, Madhwal S, Cywinski J, Lopez R, Eghtesad B et al.| title=Cumulative risk of cardiovascular events after orthotopic liver transplantation. | journal=Liver Transpl | year= 2012 | volume= 18 | issue= 3 | pages= 370-5 | pmid=22140067 | doi=10.1002/lt.22468 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22140067  }}</ref>  
* Coronary heart disease is common after liver transplantation. 
* Factors that have been associated with cardiovascular events include older age at transplantation, male sex, post-transplantation diabetes, post-transplantation hypertension, history of coronary artery disease, and use of mycophenolate mofetil.
* Ten-year risk of cardiovascular events was 14 percent and was particularly high among those with the [[metabolic syndrome]].<ref name="pmid22140067">{{cite journal| author=Albeldawi M, Aggarwal A, Madhwal S, Cywinski J, Lopez R, Eghtesad B et al.| title=Cumulative risk of cardiovascular events after orthotopic liver transplantation. | journal=Liver Transpl | year= 2012 | volume= 18 | issue= 3 | pages= 370-5 | pmid=22140067 | doi=10.1002/lt.22468 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22140067  }}</ref>  
* Liver transplant recipients have a greater risk of cardiovascular death and ischemic events than age- and sex-matched nontransplanted patients.
* Factors that have been associated with cardiovascular events include older age at transplantation, male sex, post-transplantation [[Diabetes mellitus|diabetes]], post-transplantation [[hypertension]], history of [[Coronary heart disease|coronary artery disease]], and use of [[Mycophenolate sodium|mycophenolate mofetil]].<ref name="pmid11923689">{{cite journal| author=Johnston SD, Morris JK, Cramb R, Gunson BK, Neuberger J| title=Cardiovascular morbidity and mortality after orthotopic liver transplantation. | journal=Transplantation | year= 2002 | volume= 73 | issue= 6 | pages= 901-6 | pmid=11923689 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11923689  }}</ref>
* As an example, one study compared 1312 liver transplant recipients with age- and sex-matched controls.<ref name="pmid11923689">{{cite journal| author=Johnston SD, Morris JK, Cramb R, Gunson BK, Neuberger J| title=Cardiovascular morbidity and mortality after orthotopic liver transplantation. | journal=Transplantation | year= 2002 | volume= 73 | issue= 6 | pages= 901-6 | pmid=11923689 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11923689  }}</ref>
'''Acute and chronic renal disease (CNI)'''
'''Acute and chronic renal disease'''
* Acute and chronic kidney injuries are common in liver transplantation.<ref name="pmid12954741">{{cite journal| author=Ojo AO, Held PJ, Port FK, Wolfe RA, Leichtman AB, Young EW et al.| title=Chronic renal failure after transplantation of a nonrenal organ. | journal=N Engl J Med | year= 2003 | volume= 349 | issue= 10 | pages= 931-40 | pmid=12954741 | doi=10.1056/NEJMoa021744 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12954741  }}</ref>
* Acute and chronic kidney injuries are common in liver transplantation. For the first year following transplantation, we screen patients every two to three months with a urinalysis (including microalbumin assessment) and determination of the glomerular filtration rate (GFR). After the first year, we obtain the tests every six months.<ref name="pmid12954741">{{cite journal| author=Ojo AO, Held PJ, Port FK, Wolfe RA, Leichtman AB, Young EW et al.| title=Chronic renal failure after transplantation of a nonrenal organ. | journal=N Engl J Med | year= 2003 | volume= 349 | issue= 10 | pages= 931-40 | pmid=12954741 | doi=10.1056/NEJMoa021744 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12954741  }}</ref>
* Important contributing factors are preexisting [[chronic kidney disease]], renal failure prior to liver transplantation, [[acute tubular necrosis]] around the time of transplantation, [[hypertension]], and [[diabetes mellitus]].  
* The cause of kidney injury is multifactorial. Important contributing factors are preexisting chronic kidney disease, renal failure prior to liver transplantation, acute tubular necrosis around the time of transplantation, hypertension, diabetes mellitus, and CNI toxicity.  
* CNI-related [[Acute kidney injury|acute renal failure]] is due to renal [[vasoconstriction]] and improves with dose reduction.  
* CNI-related acute renal failure is due to renal vasoconstriction and improves with dose reduction.  
* [[Chronic renal failure|Chronic renal disease]] can also be induced by these drugs, warranting continued monitoring of the plasma [[creatinine]] concentration and [[urinalysis]].  
* Chronic renal disease can also be induced by these drugs, warranting continued monitoring of the plasma creatinine concentration and urinalysis. There are conflicting data about whether chronic nephrotoxicity in liver transplant recipients is more common with cyclosporine or tacrolimus.
* [[Nephrotoxicity]] in liver transplant recipients is more common with [[cyclosporine]] or [[tacrolimus]].
'''Metabolic bone disease'''
'''Metabolic bone disease'''
* Bone loss is an important source of morbidity in liver transplant recipients (figure 5), and we assess bone mineral density prior to transplantation and every other year after transplantation to assess for osteopenia or osteoporosis.   
* Bone mineral density is assessed prior to transplantation and every other year after transplantation to assess for [[osteoporosis]].   
* The majority of bone loss and fractures occur within the first six months following transplantation, and fractures often involve the spine.<ref name="pmid3279109">{{cite journal| author=Haagsma EB, Thijn CJ, Post JG, Slooff MJ, Gips CH| title=Bone disease after orthotopic liver transplantation. | journal=J Hepatol | year= 1988 | volume= 6 | issue= 1 | pages= 94-100 | pmid=3279109 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3279109  }}</ref>  
* The majority of [[osteopenia]] and fractures occur within the first six months following transplantation, and [[Bone fracture|fractures]] often involve the [[Spinal cord|spine]].<ref name="pmid3279109">{{cite journal| author=Haagsma EB, Thijn CJ, Post JG, Slooff MJ, Gips CH| title=Bone disease after orthotopic liver transplantation. | journal=J Hepatol | year= 1988 | volume= 6 | issue= 1 | pages= 94-100 | pmid=3279109 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3279109  }}</ref>  
* <ref name="pmid7523946">{{cite journal| author=U.S. Multicenter FK506 Liver Study Group| title=A comparison of tacrolimus (FK 506) and cyclosporine for immunosuppression in liver transplantation. | journal=N Engl J Med | year= 1994 | volume= 331 | issue= 17 | pages= 1110-5 | pmid=7523946 | doi=10.1056/NEJM199410273311702 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7523946  }}</ref>Patients transplanted for cholestatic liver disease are particularly vulnerable to the development of bone loss before liver transplantation.
* Patients transplanted for [[cholestatic liver disease]] are particularly vulnerable to the development of osteoprosis before liver transplantation.<ref name="pmid7523946">{{cite journal| author=U.S. Multicenter FK506 Liver Study Group| title=A comparison of tacrolimus (FK 506) and cyclosporine for immunosuppression in liver transplantation. | journal=N Engl J Med | year= 1994 | volume= 331 | issue= 17 | pages= 1110-5 | pmid=7523946 | doi=10.1056/NEJM199410273311702 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7523946  }}</ref>  
'''Malignancy'''
'''Malignancy'''
* The incidence of malignancy is increased in liver transplant recipients [78]. Because of the increased risk, we pursue more intensive screening than is done in the general population.
* The incidence of malignancy is increased in liver transplant recipients.
* Intensive [[Screening (medicine)|screening]] than is done in the general population.


==References==
==References==
<references />

Latest revision as of 18:42, 6 January 2018


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]

Liver trasnsplantation Microchapters

Home

Patient Information

Overview

Historical Perspective

Indications

Pre-surgical management

Choice of donor

Epidemiology and Demographics

Techniques

Complications

Acute rejection

Immune therapy

Post-surgical infection

Prognosis

Overview

Complications of liver transplantation include vascular, biliary, and immunosuppression drugs complications. Hepatic artery complications include thrombosis, stenosis, and pseudoaneurysm. IVC complications include thrombosis and stenosis, usually at the site of surgical anastomosis. Biliary complications include stenosis, fistula, obstruction, stone formation, dysfunction of the Oddi sphincter, and recurrent biliary disease. Complications of immunosupression include infections, metabolic syndrome, hypertension, diabetes mellitus, obesity, dyslipidemia, coronary heart disease, acute and chronic renal disease, metabolic bone disease, and malignancy.

Post-surgical complications

Vascular Disorders

Hepatic Artery

Thrombosis

Stenosis

Portal Vein

  • Portal vein thrombosis occurs in about 1%–2% of cases.[6]
  • It most commonly results from technical problems (vessel misalignment, differences in the caliber of the anastomosed vessels, or stretching of the portal vein at the anastomotic site), previous portal vein surgery or previous thrombosis, increased downstream resistance due to a supra-hepatic stricture of the inferior vena cava (IVC), decreased portal inflow, and hypercoagulable states.
  • Portal vein stenosis has a reported incidence of 1% after liver transplantation.
  • The treatment in symptomatic cases is thrombolysis or surgery (thrombectomy, venous graft)
  • CT and MR angiography provide excellent depiction of filling defects and focal narrowing of the portal vein.
  • Transhepatic or transjugular portography may be necessary to achieve a definitive diagnosis.[7]

Inferior Vena Cava (IVC)

  • IVC complications include thrombosis and stenosis, usually at the site of surgical anastomosis.[8]
  • The anastomosis gained wide acceptance internationally and is the preferred technique for orthotopic liver transplantation at many institutions.
  • However, it is especially vulnerable to two types of complications:
  • Hemorrhage due to hepatic injury during surgery
  • Budd-Chiari syndrome due to inadequate venous drainage[9]
  • An obstruction of hepatic venous outflow may be treated with placement of a balloon-expandable stent.
  • Cross-sectional modalities such as CT and MR imaging are commonly used to confirm suspicions aroused by doppler US findings.

Biliary Disorders

Obstruction and Stenosis

  • Obstruction is the most common biliary complication both in adults and in pediatric patients and is frequently caused by stenosis at the anastomotic site.[11]
  • Anastomotic strictures usually result from fibrotic proliferation with narrowing of the biliary lumen less frequently, they are due to ischemia caused by hepatic artery thrombosis or stenosis.
  • The possible causes of nonanastomotic strictures include pretransplantation biliary diseases such as primary sclerosing cholangitis, biliary ischemia, and infection.
  • Some patients with clinical and biochemical evidence of biliary obstruction may have dilatation of both the donor and the recipient bile ducts.
  • Diffuse ductal dilatation may result from papillary dyskinesia due to devascularization or denervation of the papilla of Vater during transplantation.

Bile Leak

  • The incidence of bile leaks in liver transplant recipients is 5%.
  • Bile leaks usually occur in more than 70% occur within the 1st postoperative month.
  • Leaks occur most often at the T-tube site.
  • Bile may leak freely into the peritoneal cavity or may form a perihepatic collection.
  • Treatment includes stent placement and drainage of collections.

Ductal Ischemia

Fluid Collections

  • Seromas and hematomas are commonly observed near areas of vascular anastomosis and biliary anastomosis.
  • Pleural fluid also is a common finding.
  • US is highly sensitive for the detection of fluid collections, it is not specific.
  • CT and MR imaging are more useful for differentiating hematomas from seromas because blood has higher attenuation at CT than do other fluids.
  • The other role of imaging is to guide interventional diagnostic or therapeutic procedures.

Complications of immunosupression

Infections

  • The leading cause of mortality following liver transplantation is infection.[13]
  • Serious infections occur most frequently within the first three months post-transplantation.

Metabolic syndrome

Immunosuppressant use is associated with all aspects of the metabolic syndrome:

Hypertension

Diabetes mellitus

Obesity

  • Over one-third of patients after liver transplantation are obese.[20]
  • Approximately one-third of patients who are normal weight at the time of transplantation will become obese following transplantation.[21]
  • Body weight tends to increase during the first two years after transplantation and then stabilizes.[22]

Dyslipidemia

Cardiovascular risk

Acute and chronic renal disease (CNI)

Metabolic bone disease

  • Bone mineral density is assessed prior to transplantation and every other year after transplantation to assess for osteoporosis.
  • The majority of osteopenia and fractures occur within the first six months following transplantation, and fractures often involve the spine.[28]
  • Patients transplanted for cholestatic liver disease are particularly vulnerable to the development of osteoprosis before liver transplantation.[29]

Malignancy

  • The incidence of malignancy is increased in liver transplant recipients.
  • Intensive screening than is done in the general population.

References

  1. ↑ Tamsel S, Demirpolat G, Killi R, Aydin U, Kilic M, Zeytunlu M; et al. (2007). "Vascular complications after liver transplantation: evaluation with Doppler US". Abdom Imaging. 32 (3): 339–47. doi:10.1007/s00261-006-9041-z. PMID 16967253.
  2. ↑ Väli T, Tein A, Tiganik V, Ulst K (2013). "Vascular complications after orthotopic liver transplantation in Estonia". Transplant Proc. 45 (3): 1201–3. doi:10.1016/j.transproceed.2012.10.011. PMID 23622659.
  3. ↑ García-Criado A, Gilabert R, Bargalló X, Brú C (2002). "Radiology in liver transplantation". Semin Ultrasound CT MR. 23 (1): 114–29. PMID 11866218.
  4. ↑ Glockner JF (2001). "Three-dimensional gadolinium-enhanced MR angiography: applications for abdominal imaging". Radiographics. 21 (2): 357–70. doi:10.1148/radiographics.21.2.g01mr14357. PMID 11259700.
  5. ↑ Dodd GD, Memel DS, Zajko AB, Baron RL, Santaguida LA (1994). "Hepatic artery stenosis and thrombosis in transplant recipients: Doppler diagnosis with resistive index and systolic acceleration time". Radiology. 192 (3): 657–61. doi:10.1148/radiology.192.3.8058930. PMID 8058930.
  6. ↑ Quiroga S, Sebastià MC, Margarit C, Castells L, Boyé R, Alvarez-Castells A (2001). "Complications of orthotopic liver transplantation: spectrum of findings with helical CT". Radiographics. 21 (5): 1085–102. doi:10.1148/radiographics.21.5.g01se061085. PMID 11553818.
  7. ↑ Pieters PC, Miller WJ, DeMeo JH (1997). "Evaluation of the portal venous system: complementary roles of invasive and noninvasive imaging strategies". Radiographics. 17 (4): 879–95. doi:10.1148/radiographics.17.4.9225389. PMID 9225389.
  8. ↑ Navarro F, Le Moine MC, Fabre JM, Belghiti J, Cherqui D, Adam R; et al. (1999). "Specific vascular complications of orthotopic liver transplantation with preservation of the retrohepatic vena cava: review of 1361 cases". Transplantation. 68 (5): 646–50. PMID 10507483.
  9. ↑ Wang SL, Sze DY, Busque S, Razavi MK, Kee ST, Frisoli JK; et al. (2005). "Treatment of hepatic venous outflow obstruction after piggyback liver transplantation". Radiology. 236 (1): 352–9. doi:10.1148/radiol.2361040327. PMID 15955856.
  10. ↑ Ward J, Sheridan MB, Guthrie JA, Davies MH, Millson CE, Lodge JP; et al. (2004). "Bile duct strictures after hepatobiliary surgery: assessment with MR cholangiography". Radiology. 231 (1): 101–8. doi:10.1148/radiol.2311030017. PMID 14990819.
  11. ↑ Fulcher AS, Turner MA (1999). "Orthotopic liver transplantation: evaluation with MR cholangiography". Radiology. 211 (3): 715–22. doi:10.1148/radiology.211.3.r99jn17715. PMID 10352596.
  12. ↑ Orons PD, Sheng R, Zajko AB (1995). "Hepatic artery stenosis in liver transplant recipients: prevalence and cholangiographic appearance of associated biliary complications". AJR Am J Roentgenol. 165 (5): 1145–9. doi:10.2214/ajr.165.5.7572493. PMID 7572493.
  13. ↑ Chang FY, Singh N, Gayowski T, Wagener MM, Marino IR (1998). "Fever in liver transplant recipients: changing spectrum of etiologic agents". Clin Infect Dis. 26 (1): 59–65. PMID 9455510.
  14. ↑ Fussner LA, Heimbach JK, Fan C, Dierkhising R, Coss E, Leise MD; et al. (2015). "Cardiovascular disease after liver transplantation: When, What, and Who Is at Risk". Liver Transpl. 21 (7): 889–96. doi:10.1002/lt.24137. PMID 25880971.
  15. ↑ Laish I, Braun M, Mor E, Sulkes J, Harif Y, Ben Ari Z (2011). "Metabolic syndrome in liver transplant recipients: prevalence, risk factors, and association with cardiovascular events". Liver Transpl. 17 (1): 15–22. doi:10.1002/lt.22198. PMID 21254340.
  16. ↑ Taler SJ, Textor SC, Canzanello VJ, Wilson DJ, Wiesner RH, Krom RA (1995). "Loss of nocturnal blood pressure fall after liver transplantation during immunosuppressive therapy". Am J Hypertens. 8 (6): 598–605. doi:10.1016/0895-7061(95)00077-3. PMID 7544983.
  17. ↑ Textor SC, Canzanello VJ, Taler SJ, Schwartz L, Augustine J (1995). "Hypertension after liver transplantation". Liver Transpl Surg. 1 (5 Suppl 1): 20–8. PMID 9346597.
  18. ↑ Mangray M, Vella JP (2011). "Hypertension after kidney transplant". Am J Kidney Dis. 57 (2): 331–41. doi:10.1053/j.ajkd.2010.10.048. PMID 21251543.
  19. ↑ Younossi Z, Stepanova M, Saab S, Trimble G, Mishra A, Henry L (2015). "The association of hepatitis C virus infection and post-liver transplant diabetes: data from 17 000 HCV-infected transplant recipients". Aliment Pharmacol Ther. 41 (2): 209–17. doi:10.1111/apt.13027. PMID 25413020.
  20. ↑ Bianchi G, Marchesini G, Marzocchi R, Pinna AD, Zoli M (2008). "Metabolic syndrome in liver transplantation: relation to etiology and immunosuppression". Liver Transpl. 14 (11): 1648–54. doi:10.1002/lt.21588. PMID 18975273.
  21. ↑ Canzanello VJ, Schwartz L, Taler SJ, Textor SC, Wiesner RH, Porayko MK; et al. (1997). "Evolution of cardiovascular risk after liver transplantation: a comparison of cyclosporine A and tacrolimus (FK506)". Liver Transpl Surg. 3 (1): 1–9. PMID 9377752.
  22. ↑ Everhart JE, Lombardero M, Lake JR, Wiesner RH, Zetterman RK, Hoofnagle JH (1998). "Weight change and obesity after liver transplantation: incidence and risk factors". Liver Transpl Surg. 4 (4): 285–96. PMID 9649642.
  23. ↑ Liu LU, Schiano TD (2007). "Long-term care of the liver transplant recipient". Clin Liver Dis. 11 (2): 397–416. doi:10.1016/j.cld.2007.04.003. PMID 17606214.
  24. ↑ Gisbert C, Prieto M, Berenguer M, Bretó M, Carrasco D, de Juan M; et al. (1997). "Hyperlipidemia in liver transplant recipients: prevalence and risk factors". Liver Transpl Surg. 3 (4): 416–22. PMID 9346772.
  25. ↑ Albeldawi M, Aggarwal A, Madhwal S, Cywinski J, Lopez R, Eghtesad B; et al. (2012). "Cumulative risk of cardiovascular events after orthotopic liver transplantation". Liver Transpl. 18 (3): 370–5. doi:10.1002/lt.22468. PMID 22140067.
  26. ↑ Johnston SD, Morris JK, Cramb R, Gunson BK, Neuberger J (2002). "Cardiovascular morbidity and mortality after orthotopic liver transplantation". Transplantation. 73 (6): 901–6. PMID 11923689.
  27. ↑ Ojo AO, Held PJ, Port FK, Wolfe RA, Leichtman AB, Young EW; et al. (2003). "Chronic renal failure after transplantation of a nonrenal organ". N Engl J Med. 349 (10): 931–40. doi:10.1056/NEJMoa021744. PMID 12954741.
  28. ↑ Haagsma EB, Thijn CJ, Post JG, Slooff MJ, Gips CH (1988). "Bone disease after orthotopic liver transplantation". J Hepatol. 6 (1): 94–100. PMID 3279109.
  29. ↑ U.S. Multicenter FK506 Liver Study Group (1994). "A comparison of tacrolimus (FK 506) and cyclosporine for immunosuppression in liver transplantation". N Engl J Med. 331 (17): 1110–5. doi:10.1056/NEJM199410273311702. PMID 7523946.
Retrieved from "https://www.wikidoc.org/index.php?title=Liver_transplantation_complications&oldid=1428053"