The document provides an extensive overview of liver transplantation, detailing its history, types of donors and grafts, organ viability, and ethical issues. It discusses various clinical considerations, indications, contraindications, and outcomes in liver transplantation, along with specific attention to pediatric transplantation and the management of patients awaiting surgery. Additionally, it examines the regulatory aspects of organ transplant laws, particularly in India, and outlines the assessment processes for candidates and donors in the transplantation framework.

1. LIVER TRANSPLANTATION
 Moderator – Dr. Mandeep Singh, Dr. Prabhjot kaur
 Presenter – Dr. Venu Goyal
 Date – 02/11/2020

2. CONTENTS
History of transplantation
Types of donors and grafts
Organ viability
Ethical and constitutional issues
History of liver transplantation
Indications and contraindidcations
General and specific liver disease considerations
Pediatric transplantation
Pre anaesthetic and system oriented assessment
Donor work up
Anatomic variations
Small-for-size syndrome
DDLT
LDLT
Rejection and immunosuppression
Outcomes

3. ORGAN TRANSPLANTATION

4. HISTORY OF TRANSPLANTATION
1869 – first skin sutograft transplantation by Carl Bunger.
Bunger did rhinoplasty for syphilis with graft from inner
thigh.
1905 – first successful cornea transplant.
1908 – first skin allograft transplantation
1950 – first successful kidney transplant
1955 – first heart valve allograft into descending aorta
1963 – first successful lung transplant
1998 – first successful hand transplant
1999 – first successful tissue engineered bladder transplanted

5. TYPES OF DONORS
Living donor
Cadaveric or brain dead donors
Natural death donors

6. TYPES OF GRAFTS
Autograft –
Transplant of tissue to the same person.
Eg.– skin grafts and vein grafts.
Allograft –
Transplant b/w two genetically non-identical members of same
species.
Most human tissue and organ transplants.
Isograft –
Tissue is transplanted from donor to a genetically identical
recipient.
Eg: identical twins.
Do not trigger an immune response.
Xenograft –
Transplant of organs from one species to another.
Eg. Porcine heart valve.

7. Domino transplants –
as in CF patients, lung and heart from a deceased donor to CF
patient and heart from CF patient to heart ds patient.
ABO incompatible transplants –
as infants (under 12 months of age)do not have well-developed
immune system

8. TYPES OF TRANSPLANTS -
Organs – heart, kidney, liver, lung, pancreas, stomach and intestine
Tissues – cornea, bone, tendon, skin, pancreas islets, heart valves,
nerves and veins
Cells – bone marrow and stem cells
Limbs – hands, arms and feet
Multi-organ transplants – include lungs and heart or pancreas and
kidney

9. ORGANS AND TISSUES
TRANSPLANTED
From deceased donor only – heart, pancreas, stomach, penis, hand,
large intestine and cornea
From deceased and living donor – bone, heart valve, blood and
blood products, kidney, lung, small intestine and testis
Deceased or autograft – blood vessels
Living or autograft – bone marrow/ adult stem cell

10. ORGAN VIABILITY
Kidney – 30 hrs or less storage time
Pancreas and liver – less than 12 hrs
Heart and lungs – less than 6 hrs
- Preservation is done in chilled solution???????

11. TRANSPLANTATION OF HUMAN
ORGANS ACT (THO)
Passed in 1994
Defines about - regulation of removal of human organs and its
storage and regulation for transplantation for therapeutic purposes
and prevention of commercial dealings.

12. Main provisions (with amendments of 2014)
1. Brain death identified as a form of death and criteria for brain
death certification defined.
2. Allows transplantation from living donors and cadavers.
3. Regulatory and advisory bodies for monitoring transplantation
activity and their constitution defined.
4. The government shall maintain registry of donors and recipients.

13. REASONS FOR DONATION AND
ETHICAL ISSUES
Living related donors –
 when donors have emotional investment.
 Includes “paired exchange” technique.
Good Samaritan or ‘altruistic” donation –
 Recipient has no prior affiliation with the donor.
 Current allocation system does not assess a donor’s motive.
Financial compensation –
 legalized in certain parts of world.
 In Chennai, fishermen sold their kidneys after their livelihood was destroyed
by Indian Ocean tsunami in 2004.
Forced donation –
 lack of public organ donation program in China is used as justification.
Mostly from people deemed undesirable, such as prison populations.

15. ALLOCATION OF ORGANS
National Organ Transplant Act (NOTA) created Organ procurement
and Transplantation Network (OPTN)
Principles of primary importance –
1. Utility – maximization of net benefit to the community
2. Justice – fair pattern of distribution of nebefits??????
3. Respect for persons - including respect for autonomy

16. Organ allocation scores based on medical urgency –
1. Liver – MELD score and Child-Turcotte-Pugh score
2. Lungs – Lung Allocation Score (LAS)
3. Kidney – Estimated Post Transplant Survival (EPTS) score

17. ORGAN TRANSPLANTATION IN
INDIA
India’s 1st transplant – kidney transplant in 1970s
Approx 5000 kidneys, 1000livers and 50 hearts transplanted
annually in India.
India has a poor organ donation rate – 0.26 per million
Required – 1 per million-donation rate
First deceased donor liver transplantation – in 1995
First successful DDLT – 1998
First successful LDLT - 1998

18. LIVER TRANSPLANTATION

19. BROAD INDICATIONS OF
TRANSPLANTATION
For improved quality of life
For improved survival benefit

20. DR. THOMAS STARZL

21. HISTORY OF LIVER
TRANSPLANTAION
Liver transplant techniques were developed in 50’s and 60’s
with pivotal work of DR Thomas starzl.
First attempted human liver transplant - 1963
First successful liver transplant - 1967
Liver transplantation remained experimental till the
introduction of cyclosporine by Sir Roy Clane in 1981.
The first altruistic living liver donation - in December 2012 in St
James University Hospital Leeds.

22. EVIDENCE FOR NEED OF
TRANSPLANTATION
Advanced liver disease with MELD score more than/ equal to 15
Signs of decompensation, including ascites, encephalopathy and
renal impairment
Liver cell cancer
Development of complication such as hepatopulmonary syndrome or
portopulmonary hypertension
Intractable pruritis
Intractable encephalopathy

24. CONTRAINDIACTIONS
Absolute
Patient unfit for surgery (advanced cardiovascular / pulmonary disease)
Active sepsis
Metastatic disease
Active alcoholism
Severe intractable depression
Relative
Age
Obesity
Cholangiocarcinoma
Chronic/ refractory active infections
Poor social support
Ongoing tobacco use

25. GENERAL CONSIDERATIONS
Malnutrition d/t poor intake, dietary restrictions d/t encephalopathy,
malabsorption and disease itself. Corrections should be considered
pre-operatively.
Obesity – a/w metabolic syndrome, diabetes, cardiovascular
diseases. BMI more than 40kg/m2 is considered a relative
contraindication
Psychological assessment – to assess likelihood of non-compliance
Tobacco and other drug abuse
Age – increasing age is a/w mortality post-transplant
Previous abdominal surgery – intra-abdominal adhesions will make
surgery technically difficult
Infections – active infections are contraindication to transplantation

26. Cardiovascular diseases – CAD correction should be considered pre-
operatively
Respiratory function – causes for pulmonary abnormalities include –
Disease unrelated to liver disease (smoking)
Effects a/w liver disease (alpha 1 AT deficiency)
Respiratory conditions a/w liver disease (fibrosing alveolitis a/w primary biliary cirrhosis)
Effects of liver disease on respiratory function – pleural effusion and lung compression
Hepatopulmonary syndrome
Portopulmonary hypertension
Coexisting diseases –
Diabetes Mellitus – proliferative retinopathy, diabetic nephropathy, or autonomic neuropathy are
relative contraindications for transplantation
Hyponatremia – in advanced chronic liver disease as a consequence of injudicious diuretic therapy or
because of reduced water clearance; increased risk of central pontine myelinosis; should be corrected
before transplantation with water restriction/ renal support use
Vascular thromboses – d/t cirrhosis or underlying thrombotic tendency (myeloproliferative diseases
a/w Budd Chiari syndrome, presence of lupus anticoagulant, protein C and S deficiency, impaired
fibrinolysis)
Renal disease – combined liver and kidney transplantation can also be considered.

27. VARIANTS OF ACUTE LIVER
FAILURE
Fulminant hepatic failure
Subacute liver failure
Fulminant autoimmune hepatitis

28. FULMINANT HEPATIC FAILURE
Characterized by the onset of encephalopathy less than 7 days after the
development of jaundice.
Causes – acetaminophen overdose, viral infections (hep A, B, C, and E),
Wilson’s disease and liver disease of pregnancy.
Causes for death in FHF – cerebral edema, multiorgan failure, sepsis
(bacterial/ fungal), cardiac arrhythmia and respiratory failure.
Contraindications to transplantation in FHF include the onset of irreversible
complications i.e. irreversible cerebral edema, prolonged elevation of ICP or
presence of fixed, dilated pupils for more than 6 hrs.
Best guide to disease progression is estimation of PT or factor V.
Due to extrahepatic manifestations of FHF secondary to extensive necrotic
tissue, a two stage procedure may be considered and pt remains anhepatic
until suitable graft is available.

29. METABOLIC DISEASES
Wilson’s disease,
Haemophilia,
Hyperoxaluria requiring liver and kidney replacement,
Erythropoietic protoporphyria - likely to recur post transplant but
with decreased morbidity
Budd Chiari syndrome – transplantation considered only when portal
decompression has failed (or is not feasible) or there is established
cirrhosis.

30. CHRONIC LIVER DISEASE
Appropriate when estimated length of life in the absence of
transplantation is limited to 1 yr.
Child-Pugh and MELD scores are used for timing of transplantation.

32. PRIMARY BILIARY CIRRHOSIS
Therapies to be considered before transplantation –
 cholestyramine
 Plasmapheresis
 Antidepressants for lethargy
 Questran light (formulation without sorbitol) for cholestyramine induced nausea or diarrhea
 Extrahepatic biliary diversion
 Plasmapheresis and MARS (extracorporeal albumin perfusion)
- it does recur in allograft; at a slower rate.

34. PRIMARY SCLEROSING
CHOLANGITIS
- Premalignant condition for cholangiocarcinoma
- Cholangiocarcinoma is usually difficult to detect, therefore early
transplantation is considered.

35. ALCOHOLIC LIVER DISEASE
Candidates with good prognosis post transplant, provided,
continued abstinence from alcohol.
Abstinence period of atleast 6 months required before
transplantation
Alcoholic hepatitis is severe hepatitis characterized by high S.
bilirubin and prolonged clotting.
Patients with advanced alcoholic cardiomyopathy and pancreatitis
are unc=suitable for transplantation.

36. HEPATITIS VIRAL INFECTIONS
Hep A infection – few patients have recurrent infection in graft
Hep B infection – effective antiviral therapy has significantly reduced
need for transplantation; Hep B Ig and oral antiviral agents are
continued after transplantation.
Hep C infection – pegylated interferon and ribavirin are given pre-
operatively; seen in hemophilia patients secondary to transfusion of
infected blood.

37. HEPATOCELLULAR CARCINOMA
Accoutns for upto 30%transplants.
Other treatment approaches include – chemotherapy, resection embolization,
transarterial embolization, injection with ethanol and radiofrequency ablation.
Milan criteria (Mazzaferro et al, 1996)
- single tumor less than/equal to 5 cm, or
- 2-3 tumors none exceeding 3 cm, and
- no vascular invasion and/or extrahepatic spread
UCSF Criteria (Yao et al, 2001)
- single tumor less than / equal to 6.5 cm, or
- 2-3 lesions, none exceeding 4.5 cm, with total tumor diameter less
than/equal to 8 cm
- no vascular invasion and/or extrahepatic spread

38. Factors predicting poor outcome –
Tumor size more than 5 cm
Vascular invasion
Positive nodes
Histologic grade with poor differentiation
Serum marker – alpha fetoprotein
Transplantation in non-cirrhotic HCC livers is done for unresectable
tumors
Cholangiocarcinoma is a contraindication to transplantation because
of high recurrence rate.

39. SECONDARY LIVER CANCERS
Transplantation is not indicated for metastatic malignancy except in
carcinoid and other NETs.
Better prognostic factors – age less than 50 yrs
- primaries in lung or bowel
- pretransplant somatostatin therapy

40. PEDIATRIC TRANSPLANTATION
Indications other than those for adults – growth retardation and development of
metabolic bone disease.
Most common indication – disorders of biliary system
- biliary atresia (most common)
- Alagille syndrome
- non syndromic intrahepatic biliary hypoplasia
2nd MC indication – disorders of metabolism
- tyrosinemia
- glycogen storage diseases
- Wilson disease
- galactosuria
- gaucher syndrome

41. ASSESSMENT FOR LIVER
TRANSPLANTATION
Confirm the diagnosis of liver disease
Assess indications for liver transplant
Assess conditions that may preclude transplantation
Assess conditions that may increase the risk of procedure

42. INVESTIGATIONS
Reviewing Medical records and physical examination.
Laboratory tests –
 blood typing with antibody screen,
 hepatitis tests,
 EBV, CMV, IV testing.
Cardiac tests –
 ECG,
 ECHO,
 nuclear stress tests,
 coronary catheterization in selected cases

43. MANAGEMENT OF PATIENTS
AWAITING TRANSPLANTATION
correct vitamin deficiencies
HPHC diet
Methods to control encephalopathy while patient is continued on
high protein diet-
- lactulose
- metronidazole
- rifaximin or neomycin

44. Immunization with live/ attenuated vaccine which
cannot be given post-transplant with
immunosuppressive.
Serologic test for measles IgG
Mumps IgG
Rubella IgG
HAV IgG
HBsAb
Varicella IgG
Herpes zoster

45. Ascites
catabolic state a/w risk of SBP.
Prophylactic antibiotics such as ciprofloxacin or amoxyclav.
For severe ascites resistant to diet and diuretics, consider TIPS.
Varices
pharmacoprophylaxis with propranolol or carvedilol.
TIPS
PSC - review patients for cholangiocarcinoma/ bowel cancer
HCC patient reviewed for tumor burden.
NSAIDs avoided to reduce risk of –
- renal failure
- fluid retention
- gastritis induced haemorrhage

46. PREOPERATIVE ANESTHETIC
ASSESSMENT

47. CARDIOVASCULAR SYSTEM
Hyperdynamic circulation
In ESLD patients, with increased cardiac output secondary to decreased systemic vascular resistance and
abnormal distribution of central, splanchnic and peripheral circulation.
Cardiomyopathy
Cirrhotic, non ischemic cardiomyopathy
Treatment – sodium restriction
Also a complication of primary disease such as ethanol abuse, amyloidosis, hemochromatosis and
Wilson’s disease.
CAD
Perioperative beta-blocker has a protective effect

48. PULMONARY SYSTEM
Portopulmonary hypertension
With increased pulmonary vascular resistance and portal hypertension
Mean pulmonary artery pressure more than 25mmHg
PVR more than 240dynes/sec/cm5
Medical optimization with -
 prostaglandins (intravenous epoprostenol or inhaled iloprost)
Phosphodiestrase inhibitors (sildenafil)
ET-1 antagonists (bosentan)
Hepatopulmonary syndrome
Hypoxemia secondary to pulmonary capillary vasodilation, causing VP mismatch
Dyspnea with orthodeoxia
Liver transplantation is the only treatment
Hepatic hydrothorax
Pleural effusion more than 500ml with normal cardiac and pulmonary functions

49. HEMOSTASIS IN ESLD
Main defect – thrombocytopenia ( secondary to splenic sequestration
and decreased thrombopoetin production)
Main compensatory mechanism – increased endothelium synthesized
vWF
Reduced levels of liver synthesized factors –
Found in both acute and chronic liver failure
 plasminogen, plasmin inhibitor, thrombin activated fibrinolysis inhibitor and factor VIII
PT and aPTT– used to assess severity of synthetic dysfuntion

50. RENAL SYSTEM
Hepatorenal syndrome –
 marked by renal vasoconstriction and a severe reduction in GFR.
HRS-1 – rapid decline in renal function with multi-organ failure.
HRS-2 – benign course with milder elevation in S. creatinine.
Treatment – vasoconstrictors, renal replacement therapy.
Liver transplantation is the treatment of choice for patients with
cirrhosis and HRS.

51. DONOR WORK UP
Medical work up
BMI more than 30kg/m2 has a possibility of fatty liver.
Extensive psychological evaluation
Estimation of formula derived graft recipient volume ratio
Dtermination of future remnant liver volume
Liver biopsy may be considered in patients with steatosis
MRI with MRA, MRV and MRC may be done to define graft remnant
liver volume and vascular and biliary anatomy.

52. THE LIVER IS DIVIDED INTO EIGHT (8) SEGMENTS REFLECTING THE
EIGHT (8) MAJOR DIVISIONS OF THE PORTAL VEIN AND THE BILE DUCT
LIVER ANATOMY

54. TYPES OF LIVER GRAFTS

56. ANATOMIC VARIATIONS

57. HEPATIC ARTERY ANOMALIES

58. PORTAL VEIN
Normal – bifurcation into left and right common portal trunks.
Variation – trifurcation i.e right anterior and posterior sectional
branches arise separately

59. HEPATIC VEINS

60. GRAFT SIZE AND SMALL FOR SIZE
SYNDROME
Measure graft recipient weight ratio
SFSS – post-transplantation hepatic insufficiency presenting as
prolonged cholestasis, coagulopathy and ascites in the absence of
hepatic vascular insufficiency.
Other factors contributing to SFSS –
advanced cirrhosis
Portal hypertension
Associated hyperdynamic circulation
Optimizifn liver graft outflow reduces hyperdynamic liver injury.
Dual liver grafts – avoids SFSS

61. CADAVER DONOR
HEPATECTOMY
Incisions –
from suprasternal notch (two cavity access) to pubic symphysis
xiphoid process (one-cavity access) to pubic symphysis
Ligamentum teres, falciform ligament and gastrohepatic ligaments are
divided.
Retroperitoneal dissection done to identify left renal vein (a/w risk to injure
SMA, left renal artery and pancreas).
IMV isolated at ligament of Treitz, distally ligated.
Distal abdominal aorta exposed and encircled at bifurcation level and at level
of origin of IMA.
Porta hepatis exposed, CBD identified and encircled distally at duodenal
border and half way incised.

62. GB fundus is incised and flushed with saline until clear effluent comes from CBD.
Supraceliac aorta identified and encircled, cardiac catheter inserted at distal end
and aortic cross claping done.
Suprahepatic vena cava transected and dual perfusion with ice cold preservation
solution started.
The pericardium and left and right diaphragm around the liver are divided.
Gastroduodenal, Splenic vein, SMV and splenic artery are divided.
Transection of CBD Is completed and hilar dissectionncompleted.
The IMV is divided proximal to the renal vein and liver is excised and packed in
UW solution for preservation.

63. BACK TABLE PREPARATION OF
DONOR LIVER
Performed in preservation solution at 4 degree Celsius.
The remnant diaphragm is removed, suprahepatic vena cava
isolated.
Inferior vena cava is separated and the right adrenal vein
and other branches are ligated.
Portal vein is isolated and cannulated for flush.
Entire arterial axis is skeletonised.
**Dissection above the gastroduodenal artery should be
avoided due to potential injury to proper hepatic artery.

65. RECIPIENT HEPATECTOMY
Incison - Bilateral subcostal with midline extension.
Massive ascites - subcostal incision placed 2 to 3 cm lower.
Round ligament, left coronary, triangular ligaments and the
falciform ligament are divided.
Left lateral segment of liver ( segment 2 and 3) are reflected
towards recipients right side and gastrohepatic ligament is
divided.

66. Common hepatic artery is clamped with a bulldog clamp.
Dissection techniques of the arterial axis in the
recipient. A. Normal hepatic anatomy. RHA,
right hepatic artery; LHA, left hepatic artery;
CHA, common hepatic artery; GDA,
gastroduodenal artery. A dissection technique
that, as a first step, directly ligates (B) and
divides (C) the RHA and LHA should be avoided.
This technique can lead to a dissection of the
intima of the respective arteries due to the
preserved blood flow and subsequently result in
an occlusion of the vessels (inlay in C), which
can significantly impair the patency of the
anastomosis between the recipient and donor
arteries. (D) In contrast to this technique, at
UCLA, an atraumatic bulldog clamp (yellow) is
first placed at the CHA. Subsequently, the RHA
and LHA are ligated (E) and divided (F). In the
latter technique (D, E, and F), the risk of intima
dissection is minimized. (

67. The hepatic arteries followed by the cystic duct and cystic artery are
dissected
The isolated duct is then divided high in the hilum to ensure
sufficient length of the recipient’s duct for the later biliary
anastomosis.
Gastroduodenal artery is dissected towards the common hepatic
artery until the position of the previously placed bulldog clamp.
Portal vein dissection is completed by removing the posterior plane
of lymphatic and connective tissue.
The right lobe is elevated, and the right adrenal vein is ligated and
divided. This results in the complete separation of the posterior
aspect of the retrohepatic vena cava from the retroperitoneum. The
native liver is now ready for removal if no venovenous bypass (VVB) is
applied.

68. Vascular clamps are placed on the distal portal vein, infrahepatic and
suprahepatic vena cava.

69.  All clamps are oriented horizontally with the liver in the normal
anatomic position to avoid rotation of the vessels.
Large Satinsky vascular clamp for the suprahepatic vena cava, is
placed on the very edge of the diaphragmatic reflection to avoid
injuries to the phrenic nerve.
Lower cava is divided as proximal as possible and finally the portal
vein. The native liver is now removed. Hemostasis of the bare area is
achieved by retroperitonealization. For recipients with HCC, no
residual liver tissue of the native liver should remain at the
suprahepatic vena cava

70. VENOVENOUS BYPASS
The VVB drains the infrahepatic caval and splanchnic blood into the superior
vena cava.
Advantage :
 Maintenance of venous return and splanchnic venous drainage.
 Results in improved hemodynamic stability during the anhepatic phase .
 Reduction in mesenteric edema.
Indications:
 Patients with hemodynamic instability after clamping,
 with fulminate hepatic failure to reduce volume overload,
 with nondialysis-dependent hepatorenal syndrome.

72. IMPLANTATION OF CADAVER
WHOLE ALLOGRAFT

73. SUPRAHEPATIC VENA CAVA
ANASTOMOSIS
All hepatic vein bridges are divided to create a common
suprahepatic vena cava cuff.
After placing the donor liver into the situs, two corner stitches
are taken.
The posterior wall of the recipient and donor suprahepatic vena
cava is anastomosed from the left to the right corner.
The anterior wall anastomosis is done using the same technique
except that the suture is done from both the left and right side
and tied down in the middle.

74. INFRAHEPATIC VENA CAVA
ANASTOMOSIS
During the creation of the anastomosis, the liver is flushed
with chilled lactated Ringer’s and albumin (25 g per 1,000 mL)
solution via the portal vein cannula. The purpose of this
maneuver is to remove possible air and the high extracellular
potassium from the preservation solution (UW).
The infrahepatic vena cava anastomosis is performed in the
same fashion as the suprahepatic cava anastomosis. The suture
is not tied down to facilitate flushing and venting maneuvers

75. The caval excision is often extended distally 3-4 cm to increase
caval orifice for sufficient outflow and to prevent technical Budd
Chiari syndrome.

76. PORTAL VEIN ANASTOMOSIS
If the patient is on VVB, the bypass cannula is removed from the
portal vein and the proximal portal vein is clamped.
Avoid a redundant portal vein, which can result in kinking thus
compromising portal flow.
Portal vein is anastomosed, a fish mouth reconstruction performed in
cases of size mismatch.
Liver is reperfused through the portal vein and reperfused blood
vented through the open anterior suture line of the infrahepatic vena
cava.

77. ARTERIAL
ANASTOMOSIS
An imperfect anastomosis can result in early hepatic artery
thrombosis with graft loss.
In normal cases with type 1 anatomy of the donor and
recipient artery, the anastomosis can usually be created as end-
to-end anastomosis between a Carrel patch of the donor aorta
or artery and the common hepatic artery or branch patch of the
bifurcation of the proper hepatic and gastroduodenal artery.

78. Branch patch technique for
anastomosis of the donor celiac axis
with a Carrel patch to the longitudinally
opened recipient right and left hepatic
arteries

79. The recipient gastroduodenal artery is always ligated and divided
when the arterial anastomosis is performed with the recipient
common hepatic artery.
A replaced right hepatic donor artery stemming from the SMA (type 3
anatomy) is the most common arterial variant that requires
reconstruction.In these cases, a Carrel patch of the donor celiac artery
can be anastomosed with a Carrel patch of the donor SMA.

80. BILIARY
ANASTOMOSIS
Starts with cholecystectomy which includes the resection of the entire
donor cystic duct.
 Retrograde resection of the gallbladder from fundus downward done.
Both a duct-to-duct and a Roux-en-Y biliodigestive anastomosis can be
used for biliary reconstruction.
For choledocho-choledochostomy, donor and recipient bile duct are
shortened to an appropriate length.
 The choledocho-choledochostomy is performed as end-to-end
anastomosis. It is important to avoid redundancy and tension of the bile
duct to prevent biliary obstruction and duct necrosis, respectively.

81. If a T-tube is indicated, it is brought out of the recipient duct
approximately 1 to 1.5 cm downward the anastomotic suture
line. The T-tube exit side is narrowed with a figure-of-eight
suture .

82. Techniques of biliary duct-to-duct anastomosis with size
mismatch of donor and recipient bile duct (sketches A and C). For
equal but small-size bile ducts, the anastomotic diameter can be
increased by a site cut in each duct.

84. PIGGYBACK TECHNIQUE
The piggyback technique is used alternative to the classic
approach and preserves the native retrohepatic vena cava.
The recipient hepatectomy has a mobilization of right and left
lobes and the dissection of hepatoduodenal ligament with
division of vascular and biliary structures.
VVB is not required since venous return via IVC is preserved.
The right lobe is separated from retrohepatic vena cava and
the portal vein is clamped; the native liver is excised.

85. PRINCIPLES OF CLASSIC TECHNIQUE
(A) AND PIGGYBACK TECHNIQUE OF
ORTHOTOPIC LIVER TRANSPLANTATION
(B)

86. LIVING DONOR LIVER
TRANSPLANTATION
For LDLT, donor operation is done before recipient to ensure that
there are no obvious physical/ anatomic contraindications to safely
proceeding with donor.
In hepatic malignancy, recipient is explored first to exclude
preoperatively undetected disease that may preclude transplant.
Minimally invasive approaches in living donor hepatectomy reduce
morbidity related to abdominal wall hernia, bowel obstruction and
chronic abdominal discomfort.
Can be laproscopic/ hand assisted or robotic.

87. LEFT LATERAL SECTION
TRANSPLANT

88. OPEN DONOR PROCEDURE
Incision -
Upper midline
Left subcostal with midline extension
Left subcostal without midline extension
Bilateral subcostal with an upper midline extension
Left lateral section mobilized by dividing teres, falciform, coronary and
triangular ligaments.
Cystic duct cholangiogram done to localize left hepatic duct.
Gastrohepatic ligament (lesser omentum) divided while preserving replaced
LHA arising from left gastric artery.
Parenchymal bridge overlying umbilical fissure between segments III and IV
is divided, exposing left portal structures.
Vascular dissection is approached from LHA origin distally. Artery to
segment IV may be sacrificed as resultant ischemia is well tolerated in donor.

89.  Artery to segment IV is preserved when it arises separately from right hepatic artery

90. Full length of LPV and LHV are isolated.
Segment II and III bile duct is divided at hilar plate at base of
umbilical fissure, and distal end oversewn.
Parenchymal division is done without hepatic inflow occlusion.
LHA, LPV and LHV are divided, and graft removed.

91. LAPAROSCOPIC DONOR
PROCEDURE
Done using 5 trocar approach.
Ligaments are divided.
Left branches of HA and PV dissected and encircled.
Liver parenchyma is divided on right side of teres and falciform
ligaments, and progressed up to level of LHV.
Left bile duct is transected and proximal end sutured.
For graft extraction, a 10cm suprapubic cutaneous incision given
and retrieval beg inserted.
After graft retrieval, suprapubic incision completed,
pneumoperitoneum vented and specimen bag removed.

92. RECIPIENT PROCEDURE
Hepatectomy performed with preservation of recipient vena cava and
maximum length of HA and PV.
After hepatectomy, recipient vena cava is occluded and orifices of
hepatic veins joined to create maximum achievable graft outflow.
Graft LPV anastomosed to recipient portal bifurcation.
Hepatic arterial reconstruction performed by creating hepatic artery
bifurcation patch to match the size of graft HA.

93. LEFT LIVER TRANSPLANTATION

94. OPEN DONOR PROCEDURE
Segment IV is not devascularized.
After exposure and mobilization of left hemiliver, cholecystectomy is
performed and LHA and LPV are isolated at origin.
Left hepatic duct is divided to the left of possible anomalous entry point of
posterior right hepatic duct.
Caudate lobe is dissected off vena cava to the base of Cantlie line and
caudate vein encircled.
LHV and MHV isolated using Arantius technique.
With temporary inflow occlusion, parenchyma transected along delineation,
facilitated by hanging maneuver.
Intrahepatic MHV is divided when it enters segment IVa.
LHA and LPV ligated and divided, hepatic veins clamped and divided, and
graft removed.

95. LAPAROSCOPIC DONOR
PROCEDURE
Video accesss by abdominal wall lifting method or CO2
pneumoperitoneum.
Caudate lobe is dissected through foramen of Winslow.
Hepatic transection done under intermittent flow occlusion of right
liver with demarcation seen during occlusion.

96. RECIPIENT PROCEDURE
Caval preservation done
LHV-MHV confluence of donor and recipient are anastomosed.
Similar to all forms of LDLT

97. RIGHT LIVER TRANSPLANTATION

98. OPEN DONOR PROCEDURE
Incision –
Right subcostal with upper midline extension
B/L subcostal incision with upper midline extension
Teres and falciform ligaments are divided close to abdominal wall to
facilitate reconstruction and to prevent medial-posterior rotation and torsion
of remnant liver.
Cholecystectomy performed and cystic duct cannulated for cholangiography
for identification, marking and precise hepatic duct transection.
RHA identified and isolated from lateral border of CHD.
RPV identified and isolated from portal bifurcation.
Triangular ligament, bare area and posterior vena cava ligament divided to
mobilize right lobe.
Retrohepatic IVC mobilized, short hepatic veins ligated; veins larger than
5mm preserved.

99. Caudate process is divided over IVC, down to line of Cantlie.
Graft devascularized and flushed.
RHA clipped proximally and distally divided to allow back
bleeding
RPV clamped and divided to ensure no compromise portal
inflow to remnant liver.
RHV, significant MHV tributaries and preserved short hepatic
veins clamped and divided.
Graft removed, remaining vessels sutured, completion
cholangiogram done and reconstruction of falciform ligament
done.

100. LAPAROSCOPIC DONOR
PROCEDURES
Performed using hybrid technique of liver resection
Right lobe mobilisation –
Ligamentum teres, falciform, coronary and right triangular ligaments are divided.
Hepatic bare area is completely mobilized, right lobe elevated and retrohepatic IVC
is exposed.
Posterior vana cava ligament and short hepatic veins divided, IVC and right lobe
separated
Cholecystectomy performed.

101. Hilar dissection and liver resection –
RHA and RPV isolated
Cystic duct cannulated and cholangiogram done
Right hepatic duct transected, leaving a 5mm stumo which is oversewn
No hepatic inflow occlusion done and CVP maintained at 2-4 mmHg.
Liver parenchyma divided at Cantlie line
MHV tributaries are secured and divided
Right liver separated; RHA is ligated just lateral to CBD and transected, allowing
back bleeding from graft side.
RPV and RHV are divided.
Right lobe exteriorised from xiphoid incision.

102. IN SITU AND EX SITU
TECHNIQUE
In situ splitting minimizes cold ischemia time.
Biliary structures are better identifiable during in situ
transection.
Insitu splitting into two full hemiliver offer advantage to
apply a pringle maneuver in order to identify anatomic line
of transection.

103. RECIPIENT COMPLICATIONS
Primary non-function or poor function of the newly transplanted liver
occurs in approximately 1-5% of new transplants. If the function of the
liver does not improve sufficiently or quickly enough, the patient may
urgently require a second transplant to survive.
Hepatic artery thrombosis
Portal vein thrombosis
Biliary complications - Biliary leak
- Biliary stricture
Bleeding
Infection

104. INDUCTION AND
MAINTENANCE
IMMUNOSUPPRESSION
Triple therapy protocol – calcineurine inhibitor (tacrolimus
and cyclosporine)
- steroids
(methylprednisone)
- DNA
antimetabolite (mycophenolate mofetil).
Quadruple therapy – triple therapy plus daclizumab
(monoclonal IL 2 receptor anatagonist). For patients with
renal compromise.
Sirolimus os used in patients with intolerance to calcineurine
inhibitors or ongoing rejection with calcineurine inhibitors.

105. REJECTION
Rejection usually causes no symptoms. The first sign is usually
abnormally elevated liver laboratory test results.
Signs and symptoms, if present, include –
 Fever
 Headache
 Fatiguq
 Nausea
 Loss of appetite
 pruritis
 Dark-colored urine
 Jaundice
 Abdominal tenderness

106. OPPORTUNISTIC INFECTIONS
AND CANCER
Immunosuppression weakens a transplant recipient's
defenses against infections.
They can be divided into three periods : (1,1-6 and >6
months)
 The first month: bacteria and fungi are most common.
 first six months :Viral infections such as cytomegalovirus and other
unusual infections such as tuberculosis and pneumocystis carinii are
seen .

107. POST-TRANSPLANT
LYMPHOPROLIPHERATIVE
DISORDER (PTLD)
It is almost always associated with Epstein-Barr virus (EBV).
A common approach is therefore to give this drug,
rituximab, in conjunction with less drastic cuts of the
immunosuppression drugs.
The majority of PTLD cases can be successfully treated with
preservation of the transplanted organ.

108. OUTCOMES
Currently, the overall patient survival one year after liver
transplant is 88%. Patient survival five years after liver
transplant is 73%.
These results vary significantly based on the indication for
liver transplantation. For example, patients who underwent
transplantation for hepatocellular carcinoma had a one-year
survival of only 86% whereas patients who underwent
transplantation for biliary atresia liver disease had a one-
year survival of 94%.

109. THANK YOU