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Liver transplantation
Dr.Sarmistha
Liver Transplantation
• It is the only curative therapy for hepatic failure(either acute
or chronic). It is from either- a cadaver or a live donor.
• Starzl performed the first human liver transplant. In 1967,
Starzl successfully transplanted a liver into an 18-month-old
infant suffering from hepato cellular carcinoma.
Indications for liver transplantation
Pediatric Adult
Congenital hepatic fibrosis
Biliary atresia
Alpha 1 antitrypsin deficiency
Wilson’s disease
Gsd
Lsd
Crigler-najjar ds
Protoporphyria
tyrosinemia
Pbc
Psc
Autoimmune hepatitis
cryptogenic cirrhosis
Viral hepatitis with cirrhosis
alcoholic cirrhosis
Primary hepatocellular malignancies
Nonalcoholic steatohepatitis
fulminant hepatitis
Hepatic vein thrombosis
contraindications
Absolute Relative
Active sepsis
Active substance or alcohol abuse
Advanced cardiac disease
Extrahepatic malignancy
Metastatic malignancy
Cholangiocarcinoma
Severe obesity
Severe pulm htn
Cardiomyopathy
High viral load HIV
LDLT Vs DDLT
• The liver can regenerate within a few weeks or months to it s
original volume when upto 70% has been surgically removed
• The 30% remnant liver remains sufficiently functional to meet
the metabolic needs of the donors
• Therefore, a healthy person can donate part of his/her liver
for LT
• LDLT shortens the waiting period for recepients to receive the
donor graft
• LDLT is an elective surgery,whereas in DDLT,the procedure
often takes place in emergency
• In LDLT, it is possible to optimize the pt, in DDLT it may not be
possible d/t emergency nature of surgery.
• The quality of liver graft in LDLT is good as it is procured from
healthy donor n it has very short cold ischemic time, thereby
minimizing preservation injury
• Drawbacks of LDLT:technically more challenging operation as
native IVC has to be preserved n healthy person is subjected
to life threatening surgery
Anaesthesia for liver transplantation
• Preoperative evaluation:
• Neurologic -encephalopathy, cerebral edema
• Cardiovascular-hyperdynamic circulation, cirrhotic
cardiomyopathy, portopulmonary HTN
ECHO is the test of choice in screening for PPHTN.The
definitive diagnosis is made when mean PAP is > 25mm Hg in the
+nce of a normal PAOP and an increased PVR (>3 Wood units, or
>240 dynes/sec/cm5)
• Pulmonary: restrictive lung ds, v/q mismatch, intrapulmonary
shunts, hepatopulmonary syndrome
• Gastrointestinal: portal HTN, variceal bleeding, ascites
• Renal/metabolic:hepatorenal syndrome,acid-base
abnormalities
• Hematological:coagulopathy, anaemia
• Musculoskeletal:muscle atrophy
• The Model for End-stage Liver Disease (MELD) score is used
by the United Network for Organ Sharing (UNOS) to prioritize
patients on the waiting list for a liver transplant
• Th e MELD score = 0.957 × log e [serum creatinine
(mg/dL)] + 0.378 × log e [total serum bilirubin (mg/dL)]
+ 1.120 × log e [INR]
• A score of 20 predicts a 19.6% risk of mortality at 3 months,
whereas a score of 40 predicts a 71.3% risk of mortality at
3 months
• Premedication: BZD may be considered in elective cases but
should be avoided in pts with hepatic encephalopathy
• Monitoring: ECG, SpO2, NIBP, End-tidal CO2,Esophageal
temperature, UOP, NM monitoring, TEE,ICP
monitoring,coagulation monitoring
• Induction of anaesthesia: thiopentone: the CNS of cirrhotic
pts is sensitive to thiopentone.
Ketamine:can be used
Etomidate: safe
suxamethonium has prolonged action
• Patient positioning: supine position, with arms abducted to 70deg
lower chest n abdomen are exposed. Pressure points should be padded
• Maintenance: inhalational anaesthetics, N2O should be
avoided, avoid hypothermia
• Surgery can be divided into 3 phases:
• Pre-anhepatic phase(dissection phase)- phase of native
hepatectomy
• Begins with wide subcostal incision
• The liver is dissected so that it remains only attached by
IVC,portal vein, hepatic artery and cbd. It ends with clamps
over these vessels
• Anaesthetic problems:
• 1. massive blood loss- pre op coagulopathy and thrombocytopenia,
inc venous collaterals bn portal and systemic circulation
• Prepare multiple blood transfusions
• Rapid infusion devices-8.5 F specialized catheters infuse upto 1.5-2
l/min
• Blood salvaging devices should be available
• EACA infusion
• 2.renal: adequate iv fluid replacement,loop diuretics increase RBF
• 3.Hypocalcemia: cacl2 infusion
• 4. vasopressin infusion- 5-10U/hr is started before portal
decompression with venovenous bypass to decrease splanchnic
blood flow
• MgSo4-200mg/hr given throughout the surgery to provide
hemodynamic stability
• Anhepatic phase : this phase begins with clamping of IVC,
portal vein, hepatic arery n CBD then the liver is
excised.venovenous bypass may be done and the liver is
anastomosed. It ends with vascular anastomosis and graft
reperfusion
• Vascular anastomosis:3 options of anastomosis of IVC
A)End to end interposition of donor IVC to recipient IVC with
clamping of IVC- Std method. Supra and infrahepatic VC are
clamped and divided. Blood flow through IVC is completely
interrupted. A cylinder of the recipient IVC ,that is the segment
receiving the hepatic veins, is removed enbloc with the diseased
liver , often with venovenous bypass to support the circulation.
• B)End to end anastomosis of the vena cava to the hepatic
veins (piggyback method)-the diseased liver is dissected off
the IVC .the recepient IVC is thereby preserved and blood
flow is not completely interrupted , usually preventing the
need for venovenous bypass . One end of graft segment of IVC
is over sewn, and the open end is anastomosed to the
preserved recipient IVC
• C)Side to side cavo-cavostomy- the anastomosis of hepatic
arteries of the donor and recipient is performed by direct
connection
• 1.hemodynamic effects dec in VR, CO
• Venovenous bypass (vascular isolation of liver): not routinely
performed ,IVC is cannulated(via saphenous ) and portal vein
is cannulated (via inf mesenteric vein), then diverting their
blood flow (1-3l/min)away from the liver and back to the
heart via the rt axillary vein.
• Temporary inotropic support
• 2.metabolic effects hypocalcemia, hypo/hyperglycemia,
metabolic acidosis
• Immunosuppresant therapy is given during this phase
• Post-anhepatic phase- (neo-hepatic phase)(reperfusion of the
liver)- revascularization and biliary reconstruction are
established to the new liver.
• 1)air embolism:air may enter hepatic sinusoids and may
produce pulm and systemic paradoxical embolism
• Infusion of cold lactated ringer sol via portal vein n hepatic
artery of new liver
• After completion of portal n suprahepatic caval anastomosis,
but before completion of infra-hepatic caval anastomosis, the
portal vein clamp is released.
• 2.post reperfusion syndrome-hypotension,myocardial
depression,metabolic acidosis, hyperkalemia,
• 3.coagulopathy
• 4.PGE1 Infusion-10mcg/hr and is increased upto 40mcg/hr .it
increases blood flow to transplanted liver
• 5. document cold and warm ischemia time-
• Warm ischemia time – time from harvesting , in which the
vessels of donor liver are cross clamped ,until perfusion by
the cold sol of university of wisconsin,in addition to time from
placement of the new liver in recepient’s abdomen until its
reperfusion. Should be as short as possible. 1-2 hrs
• Cold ischemia time- time from perfusion by UW sol until
placement of liver in the recipient’s abdomen. Should be
<24hrs.(2)
• Neohepatic function can be estimated by the following-
• 1. appearance of liver: not distended, with sharp margin, and
soft
• 2. enhanced production of co2:early indicator of graft
function. d/t enhanced metabolism of organic acid by new
liver. Observed by a rise of ETCO2
• 3. Return of metabolic functions is indicated by improvement
of acidosis
• 4. hypokalemia occurs several hrs after reperfusion
• 5. normalization of coagulation factors
• 6.appearance of bile production
• 7. serum glucose return to normal
• 8. increase in uop
• 9. rising core temp
• 10. dec ca requirement
Postoperative management
• 1)ventilatory support: weaning should be done when
• Coagulopathy is controlled
• Neohepatic function returns to normal
• Renal function is normal
• Temp normal
• No evidence of sepsis n pulm congestion
• 2)Assessment of neohepatic function: diagnosis of rejection
by liver biopsy
• 3)immunosuppressive therapy: cyclosporin,
corticosteroids,azathioprine,OKT-3, and tacrolimus
• 4)postoperative analgesia: pt controlled analgesia,epidural/
paravertebral blocks
• 5)postoperative fluid management: maintenance fluid /NG
feeding at 1.5ml/kg/hr
• Blood, colloids, ffp are given to maintain cvp at 10-12cm
H2O,Hct at 26-32%, and PT < 23 sec
Postoperative complications
1. Primary non-functioning of the liver
2. Severe systemic infections
3. Respiratory failure
4. Metabolic n fluid disturbances-met alkalosis, hypokalemia,
fluid overload and hyperglycemia.
5. Surgical complications-persistent hemorrhage, bile leak,
stricture or thrombosis of the portal or hepatic vessels
6. Early postoperative death-d/t thrombosis of graft vessels/
Air embolism
7. Renal failure
8. Coagulation disorders- DIC and hyperfibrinolysis
Thank you

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Liver transplantation and anaesthetic management

  • 2. Liver Transplantation • It is the only curative therapy for hepatic failure(either acute or chronic). It is from either- a cadaver or a live donor. • Starzl performed the first human liver transplant. In 1967, Starzl successfully transplanted a liver into an 18-month-old infant suffering from hepato cellular carcinoma.
  • 3. Indications for liver transplantation Pediatric Adult Congenital hepatic fibrosis Biliary atresia Alpha 1 antitrypsin deficiency Wilson’s disease Gsd Lsd Crigler-najjar ds Protoporphyria tyrosinemia Pbc Psc Autoimmune hepatitis cryptogenic cirrhosis Viral hepatitis with cirrhosis alcoholic cirrhosis Primary hepatocellular malignancies Nonalcoholic steatohepatitis fulminant hepatitis Hepatic vein thrombosis
  • 4. contraindications Absolute Relative Active sepsis Active substance or alcohol abuse Advanced cardiac disease Extrahepatic malignancy Metastatic malignancy Cholangiocarcinoma Severe obesity Severe pulm htn Cardiomyopathy High viral load HIV
  • 5. LDLT Vs DDLT • The liver can regenerate within a few weeks or months to it s original volume when upto 70% has been surgically removed • The 30% remnant liver remains sufficiently functional to meet the metabolic needs of the donors • Therefore, a healthy person can donate part of his/her liver for LT
  • 6. • LDLT shortens the waiting period for recepients to receive the donor graft • LDLT is an elective surgery,whereas in DDLT,the procedure often takes place in emergency • In LDLT, it is possible to optimize the pt, in DDLT it may not be possible d/t emergency nature of surgery.
  • 7. • The quality of liver graft in LDLT is good as it is procured from healthy donor n it has very short cold ischemic time, thereby minimizing preservation injury • Drawbacks of LDLT:technically more challenging operation as native IVC has to be preserved n healthy person is subjected to life threatening surgery
  • 8. Anaesthesia for liver transplantation • Preoperative evaluation: • Neurologic -encephalopathy, cerebral edema • Cardiovascular-hyperdynamic circulation, cirrhotic cardiomyopathy, portopulmonary HTN ECHO is the test of choice in screening for PPHTN.The definitive diagnosis is made when mean PAP is > 25mm Hg in the +nce of a normal PAOP and an increased PVR (>3 Wood units, or >240 dynes/sec/cm5)
  • 9. • Pulmonary: restrictive lung ds, v/q mismatch, intrapulmonary shunts, hepatopulmonary syndrome • Gastrointestinal: portal HTN, variceal bleeding, ascites • Renal/metabolic:hepatorenal syndrome,acid-base abnormalities • Hematological:coagulopathy, anaemia • Musculoskeletal:muscle atrophy
  • 10. • The Model for End-stage Liver Disease (MELD) score is used by the United Network for Organ Sharing (UNOS) to prioritize patients on the waiting list for a liver transplant • Th e MELD score = 0.957 × log e [serum creatinine (mg/dL)] + 0.378 × log e [total serum bilirubin (mg/dL)] + 1.120 × log e [INR] • A score of 20 predicts a 19.6% risk of mortality at 3 months, whereas a score of 40 predicts a 71.3% risk of mortality at 3 months
  • 11.
  • 12. • Premedication: BZD may be considered in elective cases but should be avoided in pts with hepatic encephalopathy • Monitoring: ECG, SpO2, NIBP, End-tidal CO2,Esophageal temperature, UOP, NM monitoring, TEE,ICP monitoring,coagulation monitoring • Induction of anaesthesia: thiopentone: the CNS of cirrhotic pts is sensitive to thiopentone. Ketamine:can be used Etomidate: safe suxamethonium has prolonged action • Patient positioning: supine position, with arms abducted to 70deg lower chest n abdomen are exposed. Pressure points should be padded
  • 13. • Maintenance: inhalational anaesthetics, N2O should be avoided, avoid hypothermia • Surgery can be divided into 3 phases: • Pre-anhepatic phase(dissection phase)- phase of native hepatectomy • Begins with wide subcostal incision • The liver is dissected so that it remains only attached by IVC,portal vein, hepatic artery and cbd. It ends with clamps over these vessels • Anaesthetic problems: • 1. massive blood loss- pre op coagulopathy and thrombocytopenia, inc venous collaterals bn portal and systemic circulation
  • 14. • Prepare multiple blood transfusions • Rapid infusion devices-8.5 F specialized catheters infuse upto 1.5-2 l/min • Blood salvaging devices should be available • EACA infusion • 2.renal: adequate iv fluid replacement,loop diuretics increase RBF • 3.Hypocalcemia: cacl2 infusion • 4. vasopressin infusion- 5-10U/hr is started before portal decompression with venovenous bypass to decrease splanchnic blood flow • MgSo4-200mg/hr given throughout the surgery to provide hemodynamic stability
  • 15. • Anhepatic phase : this phase begins with clamping of IVC, portal vein, hepatic arery n CBD then the liver is excised.venovenous bypass may be done and the liver is anastomosed. It ends with vascular anastomosis and graft reperfusion • Vascular anastomosis:3 options of anastomosis of IVC A)End to end interposition of donor IVC to recipient IVC with clamping of IVC- Std method. Supra and infrahepatic VC are clamped and divided. Blood flow through IVC is completely interrupted. A cylinder of the recipient IVC ,that is the segment receiving the hepatic veins, is removed enbloc with the diseased liver , often with venovenous bypass to support the circulation.
  • 16. • B)End to end anastomosis of the vena cava to the hepatic veins (piggyback method)-the diseased liver is dissected off the IVC .the recepient IVC is thereby preserved and blood flow is not completely interrupted , usually preventing the need for venovenous bypass . One end of graft segment of IVC is over sewn, and the open end is anastomosed to the preserved recipient IVC • C)Side to side cavo-cavostomy- the anastomosis of hepatic arteries of the donor and recipient is performed by direct connection
  • 17.
  • 18. • 1.hemodynamic effects dec in VR, CO • Venovenous bypass (vascular isolation of liver): not routinely performed ,IVC is cannulated(via saphenous ) and portal vein is cannulated (via inf mesenteric vein), then diverting their blood flow (1-3l/min)away from the liver and back to the heart via the rt axillary vein. • Temporary inotropic support • 2.metabolic effects hypocalcemia, hypo/hyperglycemia, metabolic acidosis • Immunosuppresant therapy is given during this phase
  • 19. • Post-anhepatic phase- (neo-hepatic phase)(reperfusion of the liver)- revascularization and biliary reconstruction are established to the new liver. • 1)air embolism:air may enter hepatic sinusoids and may produce pulm and systemic paradoxical embolism • Infusion of cold lactated ringer sol via portal vein n hepatic artery of new liver • After completion of portal n suprahepatic caval anastomosis, but before completion of infra-hepatic caval anastomosis, the portal vein clamp is released.
  • 20. • 2.post reperfusion syndrome-hypotension,myocardial depression,metabolic acidosis, hyperkalemia, • 3.coagulopathy • 4.PGE1 Infusion-10mcg/hr and is increased upto 40mcg/hr .it increases blood flow to transplanted liver • 5. document cold and warm ischemia time- • Warm ischemia time – time from harvesting , in which the vessels of donor liver are cross clamped ,until perfusion by the cold sol of university of wisconsin,in addition to time from placement of the new liver in recepient’s abdomen until its reperfusion. Should be as short as possible. 1-2 hrs
  • 21.
  • 22. • Cold ischemia time- time from perfusion by UW sol until placement of liver in the recipient’s abdomen. Should be <24hrs.(2) • Neohepatic function can be estimated by the following- • 1. appearance of liver: not distended, with sharp margin, and soft • 2. enhanced production of co2:early indicator of graft function. d/t enhanced metabolism of organic acid by new liver. Observed by a rise of ETCO2 • 3. Return of metabolic functions is indicated by improvement of acidosis
  • 23. • 4. hypokalemia occurs several hrs after reperfusion • 5. normalization of coagulation factors • 6.appearance of bile production • 7. serum glucose return to normal • 8. increase in uop • 9. rising core temp • 10. dec ca requirement
  • 24. Postoperative management • 1)ventilatory support: weaning should be done when • Coagulopathy is controlled • Neohepatic function returns to normal • Renal function is normal • Temp normal • No evidence of sepsis n pulm congestion • 2)Assessment of neohepatic function: diagnosis of rejection by liver biopsy • 3)immunosuppressive therapy: cyclosporin, corticosteroids,azathioprine,OKT-3, and tacrolimus
  • 25. • 4)postoperative analgesia: pt controlled analgesia,epidural/ paravertebral blocks • 5)postoperative fluid management: maintenance fluid /NG feeding at 1.5ml/kg/hr • Blood, colloids, ffp are given to maintain cvp at 10-12cm H2O,Hct at 26-32%, and PT < 23 sec
  • 26. Postoperative complications 1. Primary non-functioning of the liver 2. Severe systemic infections 3. Respiratory failure 4. Metabolic n fluid disturbances-met alkalosis, hypokalemia, fluid overload and hyperglycemia. 5. Surgical complications-persistent hemorrhage, bile leak, stricture or thrombosis of the portal or hepatic vessels 6. Early postoperative death-d/t thrombosis of graft vessels/ Air embolism 7. Renal failure 8. Coagulation disorders- DIC and hyperfibrinolysis