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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5258_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Contents
- •1.1 Why Primary Care?
- •2.2.10 Infections
- •2.1 Introduction
- •2.2 Pre-transplant Evaluation
- •2.2.1 Overview
- •2.2.3 Laboratory Testing
- •2.2.4 Cardiopulmonary Screening
- •2.2.6 Dental Evaluation
- •2.2.7 Family Planning
- •2.2.11 Cancer Screening
- •2.2.12 Surgical Evaluation
- •2.2.13 Psychosocial Evaluation
- •2.2.13.1 Financial Evaluation
- •2.2.13.2 Psychiatric Evaluation
- •2.2.13.3 Medication Adherence
- •2.2.13.4 Substance Use
- •2.5.1 Transplanted Organ
- •2.5.2 Time Course
- •2.5.3 Graft Function
- •2.5.4 Complications
- •2.5.5 Medications
- •2.5.6 Serologic Status
- •2.5.7 Metabolic Complications
- •2.5.8 Examination
- •2.8 Conclusion
- •References
- •3.1 Introduction
- •3.2 Typical Immunosuppressant Course
- •3.4 Monitoring
- •3.5 Drug-Related Complications
- •3.6 Drug Interactions [18, 19]
- •3.6.1 COVID-19 Drug-Related Concerns
- •3.9 Conclusion
- •References
- •4.1 Kidney Transplant Recipients
- •4.1.1 Introduction
- •4.1.2 Pre-transplant Course
- •4.1.2.2 Pre-Transplant Treatment
- •4.1.2.3 Waiting List
- •4.1.2.4 Allocation
- •4.1.3 Anatomy
- •4.1.4 Immunosuppression Regimen
- •Alternative Immunosuppressive Strategies
- •4.1.6 Graft Function Surveillance
- •4.1.6.2 Clinical Evaluation
- •4.1.6.4 Biopsies
- •4.1.7 Allograft Dysfunction
- •4.1.7.1 Surgical Complications
- •4.1.7.2 Acute Rejection
- •4.1.7.3 Chronic Allograft Nephropathy
- •4.1.8.1 BK Nephropathy
- •4.1.8.2 Urinary Tract Infection
- •4.1.8.3 Cardiovascular Disease
- •4.1.8.4 Hyperlipidemia
- •4.1.8.5 Hypertension
- •4.1.8.6 Diabetes
- •4.1.8.7 Weight Gain
- •4.1.8.8 Post-Transplant Malignancies
- •4.1.8.9 Chronic Kidney Disease-Metabolic Bone Disease (CKD-MBD)
- •4.1.8.10 Electrolyte Abnormalities
- •4.1.8.11 Hematologic Abnormalities
- •4.2 Pancreas Transplant Recipients
- •4.2.1 Introduction
- •4.2.4 Anatomy
- •4.2.5 Immunosuppression
- •4.2.6 Pancreas Transplant Follow-Up Care
- •4.3 Conclusion
- •References
- •5.1 Introduction
- •5.2 Liver Transplant Anatomy
- •5.3.1 Typical Immunosuppressive Course
- •5.3.2 Infections
- •5.3.3 Graft Dysfunction
- •5.3.4 Vascular Complications
- •5.3.5 Biliary Complications
- •5.3.6 Allograft Rejection
- •5.4.2 Typical Immunosuppressive Course
- •5.4.4 Chronic (Ductopenic) Rejection
- •5.4.6 Late Surgical Complications
- •5.5.1 Immunosuppression Management
- •5.5.2 Immunizations
- •5.5.3 Cancer Screening
- •5.6.2 Diabetes Mellitus
- •5.6.3 Systemic Hypertension
- •5.6.4 Dyslipidemia
- •5.6.5 Chronic Kidney Disease
- •5.6.6 Infectious Disease
- •5.6.7 Mental Health
- •5.6.8 Pain Management
- •5.8 Summary
- •References
- •6.1 Introduction
- •6.2 Pre-Transplant Course
- •6.2.1 Common Indications
- •6.4 Typical Anti-Rejection Course
- •6.4.1 Induction
- •6.4.2 Maintenance
- •6.4.3 Long-Term Dose Adjustments
- •6.5 Rejection
- •6.5.1 Pathophysiology
- •6.5.2 Clinical Presentation
- •6.5.3 Evaluation
- •6.6 Rejection Surveillance
- •6.6.1 Cellular Rejection
- •6.6.2 Antibody-Mediated Rejection
- •6.3 Anatomy
- •6.3.1 Anastomoses (Bicaval Method)
- •6.3.2 Denervation
- •6.3.2.1 Pericardium
- •6.6.3 Overall Rejection Surveillance Strategies
- •6.7 Graft Function Surveillance
- •6.8.1 Cardiac Allograft Vasculopathy (CAV)
- •6.8.2 De Novo Coronary Atherosclerosis
- •6.8.3 Arrhythmias
- •6.8.4 Valvular Disease
- •6.9.2 Cardiovascular Disease
- •6.9.3 Chronic Kidney Disease
- •6.9.4 Cancer
- •6.9.5 Hypertension
- •6.9.6 Diabetes
- •6.9.7 Infectious Endocarditis Prophylaxis
- •6.9.8 Pregnancy
- •6.9.10 Diet
- •6.10 Case Studies
- •6.10.2 Case Study
- •6.10.4 Case Study
- •6.10.6 Case Study
- •6.10.8 Case Study
- •6.10.10 Case Study
- •6.11 Conclusion
- •References
- •7.1 Introduction
- •7.2 Lung Transplant Anatomy
- •7.3.1 Induction
- •7.3.2 Maintenance
- •7.4.1 Monitoring/Spirometry
- •7.4.2 Monitoring/Surveillance Bronchoscopy
- •7.5 Post-Lung Transplant Pulmonary Complications
- •7.5.1 General Issues
- •7.5.2 Acute Rejection
- •7.5.3 Airway Complications
- •7.5.4 Infections
- •7.5.6 Chronic Lung Allograft Dysfunction (CLAD)
- •7.6.1 General Issues
- •7.6.3 Malignancy
- •7.7 Conclusions
- •References
- •8.1 Introduction
- •8.3 Respiratory Infections
- •8.3.1 Diagnostic Considerations
- •8.3.2 Respiratory Viral Illnesses
- •Clinical Presentation
- •Treatment
- •Prevention
- •Clinical Presentation
- •Diagnosis
- •Treatment
- •Prevention
- •8.3.2.3 Other Respiratory Viral Infections
- •Herpes Viruses
- •8.3.2.4 Bacterial Pneumonia
- •8.3.2.5 Mycobacterial Infections
- •8.3.2.6 Fungal Pneumonia
- •8.4 Gastrointestinal Infections
- •8.4.1 Diagnostic Considerations
- •8.4.2.1 Epidemiology
- •8.4.2.2 Diagnosis
- •8.4.3 Cytomegalovirus
- •8.4.3.1 Risk Factors
- •8.4.3.2 Diagnosis
- •8.4.3.3 Treatment
- •8.4.5 Parasites
- •8.4.6 Non-infectious Causes
- •8.4.7 Esophagitis
- •8.5 Urinary Tract Infections
- •8.5.2 Risk Factors
- •8.5.5 Diagnostic Considerations
- •8.5.6 Therapeutic Considerations
- •8.5.8 Sexually Transmitted Infections (STIs)
- •8.7.1 Diagnostic Considerations
- •8.7.3 Necrotizing Skin Infections
- •8.7.4 Infectious Vesicular Eruptions
- •8.7.6 Sexually Transmitted Infections
- •8.8 Prevention
- •8.9 Conclusion
- •References
- •9.1 Introduction
- •9.2 Respiratory Symptoms
- •9.2.1 General Approach: Cough
- •9.2.1.1 Assess Clinical Stability
- •9.2.1.2 History
- •9.2.1.3 Examination
- •9.2.2 General Approach: Dyspnea
- •9.2.2.1 Assess Clinical Stability
- •9.2.2.2 History
- •9.2.2.3 Examination
- •9.2.3 Key Points
- •9.3 Urinary Symptoms
- •9.3.1 General Approach: Urinary Symptoms
- •9.3.1.1 Assess Clinical Stability
- •9.3.1.2 History
- •9.3.1.3 Examination
- •9.3.1.4 Differential Diagnosis
- •9.3.2 Key Points
- •9.4 Gastrointestinal Symptoms: Diarrhea
- •9.4.1 General Approach
- •9.4.1.1 Assess Clinical Stability
- •9.4.1.2 History
- •9.4.1.3 Examination
- •9.4.2 Key Points
- •9.5.1 Malignancy
- •9.5.1.1 Nonmelanoma Skin Cancers (NMSC)
- •9.5.1.2 Melanoma
- •9.5.1.3 Kaposi Sarcoma
- •9.5.1.4 Merkel Cell Carcinoma (MCC)
- •9.5.2 Infection
- •9.5.3 Graft-Versus-Host Disease (GVHD)
- •9.5.4 Cosmesis
- •9.5.5 Key Points
- •9.6 Musculoskeletal Symptoms
- •9.6.1 Joint Pain: General Approach
- •9.6.1.1 Assess Clinical Stability
- •9.6.1.2 History
- •9.6.1.3 Physical Examination
- •9.6.1.4 Differential Diagnosis
- •9.6.1.5 Additional Testing
- •9.6.2 Other Musculoskeletal Symptoms
- •9.7 Constitutional Symptoms
- •9.8 Conclusion
- •References
- •10.1 Introduction
- •10.2 Epidemiology
- •10.2.1 Cancer Incidence
- •10.2.2 Cancer Mortality
- •10.2.3 Timing
- •10.3 Risk Factors
- •10.3.1 Age
- •10.3.2 Gender
- •10.3.3 Immunosuppression
- •10.3.3.1 Calcineurin Inhibitors (CNIs)
- •10.3.3.3 mTOR Inhibitors
- •10.3.3.4 Induction Immune Suppression
- •10.3.6 Oncogenic Infections
- •10.4.1 Donor Transmitted Cancer
- •10.4.2 Skin and Lip Cancer
- •10.4.3 PTLD (Post-transplant Lymphoproliferative Disorder)
- •10.4.3.1 Epidemiology
- •10.4.3.3 Risk Factors
- •10.4.3.4 Presentation
- •10.4.3.5 Treatment
- •10.4.3.6 Prognosis
- •10.4.3.7 Prevention
- •10.4.4 Lung Cancer
- •10.4.6 HPV-Associated Cancer
- •10.4.8 Thyroid Cancer
- •10.4.9 Hepatobiliary Cancer
- •10.4.10 Colorectal Cancer
- •10.4.11 Kaposi’s Sarcoma
- •10.5.1 Non-HPV Associated Gynecologic Cancers
- •10.5.2 Breast Cancer
- •10.5.3 Prostate Cancer
- •10.9 Conclusion
- •References
- •11.1 Introduction
- •11.2 Cardiovascular Disease
- •11.2.1 Epidemiology
- •11.2.2 Pathophysiology
- •11.2.3 Screening
- •11.3 Diabetes Mellitus
- •11.3.1 Epidemiology
- •11.3.2 Pathophysiology
- •11.3.3 Screening
- •11.4 Chronic Kidney Disease
- •11.4.1 Epidemiology
- •11.4.2 Pathophysiology
- •11.4.3 Screening
- •11.5.1 Epidemiology
- •11.5.2 Pathophysiology
- •11.6 Gout
- •11.6.1 Epidemiology
- •11.6.2 Pathophysiology
- •11.6.3 Screening/Surveillance
- •11.6.5 Treatment
- •11.6.6 Prevention
- •11.7 Osteoporosis
- •11.7.1 Epidemiology
- •11.7.2 Pathophysiology
- •11.7.3 Screening
- •11.7.4 Prevention
- •11.7.5 Treatment
- •11.8 Conclusion
- •References
- •12.1 Pre-transplant Mental Health
- •12.1.4 Pre-transplant Pharmacology Considerations
- •12.3 Mental Health Disorders Post-transplant: Management
- •12.3.1.1 Before Transplant
- •12.3.1.2 Early Post-transplant
- •12.3.1.3 Many Years Post-transplant
- •12.11 Conclusion
- •References
- •13.1 Introduction
- •13.2 Pre-conception Counseling
- •13.2.1 Pregnancy Timing
- •13.2.3 Medication Management
- •13.2.4 Cytomegalovirus (CMV) Infection Prevention
- •13.3 Contraception
- •13.5 Pregnancy
- •13.6 Menopause
- •13.7 Osteoporosis
- •13.8 Gynecologic Cancers
- •13.9 Conclusion
- •References
- •14.1.1 Skin Cancer Screening
- •14.1.2 Cervical Cancer Screening
- •14.1.3 Anal Cancer Screening
- •14.1.5 Colorectal Cancer Screening
- •14.3 Metabolic Bone Disease
- •14.3.1 All Solid Organ Transplant Recipients—History
- •14.5 Safe Living Practices
- •14.5.1.1 Immunizations
- •14.5.1.2 Travel Precautions
- •14.6.1 Behavioral Health
- •14.6.2 Substance Use
- •14.7 Conclusion
- •References
- •15.1 Introduction
- •15.2 The Continuity Care Provider
- •15.3 Vaccination
- •15.3.1 Post-Transplant Vaccination
- •15.4.1 Cytomegalovirus (CMV)
- •15.4.2 Epstein Barr Virus (EBV)
- •15.4.3 Polyomaviruses
- •15.6 Development
- •15.9 Conclusion
- •References
- •16.3 Advance Care Planning
- •16.3.1 Advance Directives
- •16.4.1 Pain
- •16.4.2 Dyspnea, Cough
- •16.4.4 Edema
- •16.6 Transplant Failure
- •16.7 Conclusion
- •References
- •17.1 Introduction
- •17.1.1 Epidemiology
- •17.1.2 Terminology
- •17.3.1 Estrogen
- •17.3.1.2 Drug Interactions
- •17.3.1.4 Timing
- •17.3.3 Progestins
- •17.3.3.2 Drug Interactions
- •17.3.4 Gonadotropin-Releasing Hormone (GnRH) Agonists
- •17.3.4.2 Drug Interactions
- •17.3.5 Testosterone
- •17.3.5.2 Drug Interactions
- •17.6 Mental Health
- •17.7 Conclusion
- •References
- •Index

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4 Primary Care of the Adult Kidney Transplant and Kidney-Pancreas Transplant…

111© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2025
C. J. Wong (ed.), Primary Care of the Solid Organ Transplant Recipient,
https://doi.org/10.1007/978-3-031-98076-3_5
Chapter 5
Primary Care oftheAdult Liver
Transplant Recipient
CourtneyL.Tuegel, LaurenA.Beste, andAnneM.Larson
5.1 Introduction
Cirrhosis and chronic liver disease affects 1.7 billion individuals worldwide as of
2021, a 22.4% increase since 2010 [1]. Chronic liver disease and cirrhosis was the
tenth leading cause of death in the USA in 2022 [2]. The liver is the second most
commonly transplanted solid organ in the USA, representing roughly one-fth of
solid organ transplants since 1999 [3]. Liver transplant activity has increased 52%
in the past decade, with the demand for liver transplantation—just over 25,000 can-
didates on the wait list in 2022—far exceeding the supply of ~9800 deceased donor
organs [4]. Despite the high demand, the number of newly listed liver transplant
candidates has decreased in recent years and 54.5% of candidates on the wait list
receive a transplant within 1year, with 61% of transplant recipients having waited
less than 90days [4]. Contrasting with dialysis for kidney failure, no mechanical
organ substitutes exist for end-stage liver failure.
The most common indications for adult liver transplantation include chronic
liver failure, hepatocellular carcinoma, and acute liver failure (most often
due to toxic ingestion). The most common etiologies of chronic liver disease in the
United States include hepatitis C virus infection (HCV), metabolic associated
C. L. Tuegel (*) · L. A. Beste
Division of General Internal Medicine, Department of Medicine, University of Washington,
Seattle, WA, USA
General Medicine Service, VA Puget Sound Healthcare System, Seattle, WA, USA
e-mail: courtly@uw.edu; Lab25@uw.edu
A. M. Larson
Division of Gastroenterology, Department of Hepatology and Liver Transplantation,
University of Washington, Seattle, WA, USA
e-mail: amlarson@uw.edu

112
0
5
10
15
20
25
30
35
40
45
2010 2012 2014 2016 2018 2020 2022 2024
Percentage
Year
Total liver transplants by clinical diagnosis
Acute Liver Failure
HCV
ALD
Chol
HCC
Other/unknown
Fig. 5.1 Total liver transplants by clinical diagnosis. ALD: alcoholic liver disease; HCV: hepatitis
C virus, Chol: cholestatic, HCC: hepatocellular carcinoma, other: includes metabolic associated
steatohepatitis. (Data from: Scientic Registry of Transplant Recipients. Available at: https://srtr.
transplant.hrsa.gov/annual_reports/Default.aspx. Accessed September 9, 2024)
steatohepatitis (MASH), and alcohol-related liver disease (ALD). HCV has histori-
cally been the leading indication for liver transplantation, but the advent of direct
acting antiviral therapies has led to a decline in the proportion of transplants per-
formed for HCV, surpassed by ALD (40.8% of adult liver transplants in 2022) and
MASH (at least 19.9% of adult liver transplants in 2022) [4–6]. Recent trends sug-
gest that MASH is the most rapidly increasing indication for liver transplantation
[6] (Fig.5.1).
Survival after liver transplantation is generally excellent, with 1- and 5-year post-
transplant survival at 93.2% and 80.2%, respectively, while the rate of 10-year sur-
vival is 64.3% [4]. Post-liver transplant complications are divided into acute
(3–6months post-liver transplant) and chronic or long term. Liver transplant centers
typically bear responsibility for managing the patient’s immunosuppressive regi-
men and any hepatic or biliary complications that arise after liver transplantation
[7]. Primary care providers (PCPs) should expect to manage the long-term meta-
bolic side effects of immunosuppression, and preventive care such as vaccinations
and cancer screenings. In addition, PCPs may be the rst point of contact for patients
when new symptoms arise.
5.2 Liver Transplant Anatomy
Deceased donor transplants comprise 93.7% of all liver transplants in the US [4].
• The donor liver is placed in the orthotopic position (same location as the
native organ).
C. L. Tuegel et al.

113
Fig. 5.2 Anatomy and
blood supply of the
transplanted liver.
(Reproduced with
permission from: Berry
PA, Melendez HV, Wendon
JA. (2010) Postoperative
Care of the Liver
Transplant Patient. In:
O’Donnell JM, Nácul FE
(eds) Surgical Intensive
Care Medicine. Springer,
Boston, MA)
• Four surgical anastomoses must be created between the donor allograft and the
recipient to implant the new liver: inferior vena cava/hepatic veins, hepatic artery,
portal vein, and common bile duct (Fig.5.2).
– There are two predominant caval reconstructions: the traditional technique
(caval replacement, in which the relevant portion of the recipient’s inferior
vena cava is resected and replaced with the donor portion; Fig.5.3a) and the
piggyback technique (Fig.5.3b, c).
– The caval technique has largely been supplanted by the piggyback technique.
The donor vena cava is closed inferiorly. The superior portion of the donor
cava (including the hepatic veins) is anastomosed end-to-end to the recipient
hepatic vein (Fig.5.3b) or side-to-side (Fig. 5.3c) with the recipient vena
cava. This technique reduces the need for veno-venous bypass.
• Both the donor and recipient gallbladder are removed at the time of surgery.
• In some settings, hepaticojejunostomy with Roux-en-Y reconstruction is
necessary.
• Arterial or venous thromboses, stricture, or leakage from any of these anastomo-
ses are a common source of early post-transplant complications.
Living donor liver transplants (i.e., transplanting a portion of a healthy person’s
liver) are performed less often due to risk to the donor, including death. Segmental
living donor liver transplantation is occurring with increasing frequency, however,
accounting for 603 liver transplants in 2022 [4]. The surgical anastomoses vary in
this type of transplant depending on the hepatic segment used. This review will
focus on transplantation from deceased donors in which the entire donor organ is
implanted.
5 Primary Care oftheAdult Liver Transplant Recipient

114
a
b
c
Fig. 5.3 Variations in caval reconstruction. (a) Classic. (b) Piggyback hepatic vein. (c) Side to
side. (Reproduced with permission from: Chan T, DeGiolamo K, Chartier-Plante S, Buczkowski
AK. (2017) Comparison of three caval reconstruction techniques in orthotopic liver transplanta-
tion: a retrospective review. Am J Surg 2013:5:943–949)
5.3 Early Posttransplant Period—First 12Months
Transplant recipients are closely monitored as inpatients during the immediate post-
operative period for hemodynamic stability and acute post-transplant complica-
tions. This management is carried out by a multidisciplinary team that includes
surgeons, hepatologists, intensivists, pharmacists, dietitians, and nursing staff. In
addition to the perioperative complications inherent in any surgery, such as bleed-
ing, infection, or poor wound healing, liver transplant recipients have additional
early risks. Very early post-transplant complications, within 3 months, include
opportunistic infection, graft dysfunction, transplant-related surgical complications
C. L. Tuegel et al.

115
such as hepatic vascular thrombosis or biliary leaks, acute rejection, and other organ
dysfunction (e.g., renal, pulmonary, neurologic) [8].
5.3.1 Typical Immunosuppressive Course
Transplant centers vary in their choice of immunosuppression in the rst-year post-
transplant. Induction therapy is used during the rst week post-liver transplant in
some recipients, depending on the transplant center protocol. Induction therapies
include antilymphocyte sera such as antithymocyte globulin, or monoclonal anti-
bodies (e.g., basiliximab,) which act by blocking interleukin-2 receptors.
Corticosteroids are less commonly used than in the past, and if used are tapered over
the next 3–12months.
5.3.2 Infections
Infection remains a signicant risk in the setting of liver transplantation. Sources of
infection include (a) the donor organ, (b) reactivation of prior infection in the recipi-
ent, and (c) de novo infection by exogenous or endogenous organisms. During the
rst month, infections are typically nosocomial. Viral infections (e.g., cytomegalo-
virus [CMV], Epstein-Barr Virus [EBV]) predominate during the second to sixth
month post-transplant, followed by fungal, bacterial and parasitic infections [9].
Because of the risk of opportunistic infection, post-liver transplant patients rou-
tinely receive viral, bacterial and fungal prophylaxis. Protocols vary by institution.
In general, antibacterial prophylaxis is provided for Pneumocystis jirovecii. Fungal
prophylaxis is used against candida species and tailored by the center if endemic
fungi are prominent (i.e., histoplasmosis, cryptococcus). CMV prophylaxis is typi-
cally given for seronegative recipients receiving CMV-positive livers, or those
undergoing induction immunosuppression with a T-cell specic agent such as thy-
moglobulin [10, 11]. Acyclovir prophylaxis for herpes simplex is given if CMV
prophylaxis is not used. The prophylactic agents are generally discontinued over the
next 3–12months, depending upon center protocol. Following the sixth month post-
liver transplantation, infections are predominantly community-acquired and similar
to those of the general population (see Chap. 8).
5.3.3 Graft Dysfunction
Primary nonfunction is one of the most serious immediate post-liver transplant
complications, occurring in up to 10% of recipients. In this circumstance, the graft
fails to function immediately following reperfusion, and the patient develops acute
5 Primary Care oftheAdult Liver Transplant Recipient

116
liver failure and must be urgently retransplanted. Additionally, subacute graft failure
can develop in 6.4% of liver transplant recipients by 6months and 8.4% by 1year
and may require retransplantation [4]. Because early graft dysfunction may be
asymptomatic, liver function is carefully monitored with frequent laboratory studies
and imaging. Timing of studies varies, but in general laboratory testing ranges from
weekly to every 3months depending on time following transplant. Imaging is gen-
erally done every 3–6months the rst year, or for cause, and then yearly. Protocol
liver biopsies, used in the past to assess for rejection, are no longer performed.
Factors associated with graft dysfunction include donation after cardiac death,
donor macrovesicular steatosis, total ischemia time >10h, reperfusion damage,
older donor age (>60years), and recurrent primary liver disease [12].
5.3.4 Vascular Complications
Post-transplant arterial complications include thrombosis, stenosis, pseudoaneu-
rysm, and arterial rupture. Hepatic arterial pseudoaneurysms predispose to life-
threatening hemorrhage and may require urgent endovascular or surgical
intervention. Hepatic artery thrombosis (HAT) occurs in roughly 3.5% of liver
transplant recipients and is a leading cause of early graft failure, requiring retrans-
plantation in up to 83% of cases [13]. The liver has a dual blood supply from both
portal vein and hepatic artery, with only the hepatic artery carrying oxygenated
blood. Even transient interruption of hepatic arterial ow may result in anoxic injury
to the sensitive small bile ducts, especially if occurring within 4 weeks post-
transplant (“early” HAT). The clinical consequences of HAT vary widely. Early
HAT often leads to ischemia and necrosis of the allograft. Thrombolysis, thrombec-
tomy, or surgical intervention may be attempted followed by anticoagulation; how-
ever, failure to recanalize the artery necessitates urgent retransplantation.
If thrombosis occurs later, it typically leads to biliary complications with pre-
served hepatic synthetic function. Complications of HAT include bile duct necrosis,
intrahepatic bilomas, ischemic cholangiopathy, secondary biliary cirrhosis, and
death unless corrected rapidly through surgical or interventional radiologic inter-
vention. Therefore, most centers monitor laboratory results and routine duplex
ultrasounds of the hepatic vessels in the early post-transplant setting (e.g., day 1 and
day 5–7 post-transplant). Late hepatic artery thrombosis can present years after
transplantation, although it may not require retransplantation if a collateral blood
supply has developed. Late hepatic artery thrombosis is most often detected by rou-
tine duplex ultrasound or laboratory studies.
Portal vein thrombosis or stenosis are rare complications, and each occur in <3%
of liver recipients. They are associated with increased risk of graft failure as well as
increased mortality, but are largely treatable with anticoagulation and percutaneous
radiological intervention [13]. Severe cases may result in portal hypertension with
its subsequent complications of ascites and varices. The hepatic veins and inferior
vena cava may also develop thromboses or stenoses, but this is less common.
C. L. Tuegel et al.
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