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ANESTHESIA FOR LIVER
RESECTION
Dr Kiran Rajagopal DA DNB
Anaesthesiologist
Indications
 Removal of hepatic metastases from colorectal carcinoma
 Removal of primary hepatic tumours such as hepatocellular
carcinomas or biliary tumours such as cholangiocarcinomas
 Following trauma to the liver.
 Removal of benign liver tumours(hepatic adenoma), liver cysts
 Live donor liver transplantation.
 Segmental resections may be required as part of
hepaticojejunostomy procedures for high bile duct injuries
Laparoscopic hepatectomy
 Far less common than open procedures
 Recognized for
 liver cysts
 peripheral solitary metastases
 hepatocellular carcinoma.
Surgical Course
Access Mobilisation
Inflow
control
Outflow
control
Parenchymal
transection
 Access: incision is upper midline, extending to right
subcostal region (Lexus incision).
 Mobilization: division of the triangular ligaments (frees
the liver from the diaphragm). Mobilization of the vena
cava. cholecystectomy done
 Inflow control: obtained by a variety of techniques
(eg. dissection of the liver hilum with control of the portal vein and
hepatic artery, dividing the bile duct within the liver substance. Or,
alternatively, dissection of the intrahepatic inflow pedicle etc)
 Outflow control: classically, the hepatic vein is divided
extrahepatically, but can also be divided within the liver
during parenchymal transection.
 Parenchymal resection:
 Before resection,CT and MRI to confirm exact
tumour location and vascular anatomy
Intra-operative ultrasound is mandatory to confirm
preoperative assessments and identify additional
lesion
 Parenchymal transection has been described using a
number of techniques.
Commonly, dissection with a clamp crushing
technique or Cavitron Ultrasonic Aspirator (CUSA)
are used to disrupt liver parenchyma, revealing
vessels and bile ducts that may then be clipped or
ligated.
 Confirmation of haemostasis and abdominal
closure
Haemostasis achieved with the use of argon
beam coagulation and fibrin glues
Recently the trend has moved away from
“anatomical resection” (respects the portal
triad) towards “non-anatomic resection”
(resection of a lesion with 1-2 cm margins,
irrespective of hepatic anatomy).
ANAESTHETIC CONCERNS
Pre operative
 Preoperative assessment should be adapted to the needs
of each individual patient, based on general
comorbidities and hepatic function.
 Patients without parenchymal liver disease are assessed
as for any major intra-abdominal operation.
 Patients with hepatic disease are at significantly
increased risk of multi-organ dysfunction, including
cardiac failure, impaired gas exchange, bleeding and
renal failure
Colorectal metastasis
 neo-adjuvant chemotherapy
 5-Fluorouracil (5-FU) with leucovorin and
oxaliplatin
Pros Cons
Neo adjuant chemotherapy
Pre operative
 Of particular concern are conditions causing an elevation
of right-side cardiac and central venous pressure (CVP)
that significantly increases the risk of intra-operative
bleeding.
 Early communication with the surgical team will identify
cases with a high risk of intra-operative bleeding, large
resection, or postoperative liver failure
Assessment of liver function
 In young patients with normal hepatic parenchyma, it is
safe to remove up to four liver segments amounting to a
50–60% resection
 survival after 80% resection is possible.
 postoperative liver failure can occur
 underlying chronic liver disease presenting for liver
resection are at high risk of postoperative liver failure
Child-Pugh scoring
 Child B &C unfit for liver resection
 indocyanine green (ICG) retention- measures liver
perfusion and biliary excretion
 Impaired clearance of ICG is suggested when more than
15% of the dose remains in the plasma 15 min after injection
Predictors of transfusion
 a) preoperative hemoglobin concentrations
below 12.5 g/dl,
 (b) tumor more than 4 cm,
 (c) need for exposure of the vena cava,
 (d) need for an associated procedure, and
 (e) cirrhosis
Intraoperative
 GA ,ETT ,CV with or without thoracic epidural
 Little evidence to favour any particular choice of
anaesthetic agent
 Hepatic clearance will be reduced after resection
 Known hepatotoxins such as halothane avoided
 Nitrous oxide should be avoided as it causes gut
distension and there is a small risk of air embolism
EPIDURAL
Benefits Risks
 Post op analgesia
 Less pulmonary
complications
 Sympathetic blockade -
low CVP reduces blood
loss and transfusion
requirements
 Post op coagulopathy
 Pre op coagulopathy
 Epidural
hematoma/abscess
 Increased total
intravenous fluid
administration
 Increased transfusion due
to haemodilution
Even in patients with pre op normal liver function and coagulation, prothrombin
time (PT) is prolonged in the majority of patients on the first and second
postoperative days and may remain abnormal for up to 5 days
Monitoring
 Minimum monitoring standards
 Invasive arterial and CVP
 Blood glucose monitoring
 Naso-gastric tube
 Temperature monitoring – warmer
 Neuro muscular monitoring
Large bore intra-venous access
A rapid infusion system should be available
Blood Loss
 Blood loss of 10 litres has been reported after liver
resection
 Large transfusions are a risk factor for major
postoperative complications and liver failure.
 Patients with cirrhosis, steatosis, and after
chemotherapy are at especially increased risk of
coagulopathy and bleeding
TECHNIQUES TO LIMIT BLOOD LOSS
Pringle maneuver
 A noncrushing clamp or a tourniquet is placed around
the structures in the porta hepatis to occlude portal
venous and hepatic arterial inflow during parenchymal
transection.
 Intermittent or continuous
 Occlusion time limited to an hour or less
 Reduce the blood loss by up to approximately 65%
CVS Effects
 MAP increase by 6%
 Cardiac output decrease by 10%
 Left ventricular afterload increase of 20–30%
 Hypotension after clamp release
Hepatic vascular control methods
1) Inflow vascular occlusion
(A) Hepatic pedicle occlusion:
(a) Continuous Pringle maneuver (CPM)
(b) intermittent Pringle maneuver (IPM)
(B) Selective inflow occlusion.
(2) Inflow and outflow vascular exclusion
(A) Total hepatic vascular exclusion (THVE)
(B) Inflow occlusion with extraparenchymal control of the
major hepatic veins: with selective hepatic vascular
exclusion (SHVE).
Inflow Vascular Occlusion
 CPM, IPM, and selective inflow occlusion
- same haemodynamic management
 Portal triad clamping -
increases systematic vascular resistance
reduces cardiac output
increases Mean arterial pressure
 On unclamping - parameters return to baseline values.
 Main source of bleeding is backflow from the
valveless hepatic veins
Low CVP
 CVP (between 2 and 5 mmHg)
-- reduces blood loss
 Limit iv fluids
 Diuretics or Nitrate infusion
 Nitroglycerin reduces CVP to the desired level during the
resection phase or when excessive oozing is observed
from the resected surface.
 After the resection – restore circulating blood volume
 PEEP increases CVP & reduce liver blood flow
 Avoid PEEP during resection phase
 15◦ Trendelenburg position can be given
-- prevents air embolism
Risks of low CVP
 Cardiovascular instability
 Air embolism
 Postoperative renal dysfunction
If urine output falls to 0.5 ml/ kg/ h or
Refractory hypotension occurs
 small colloid bouses may be given
Inflow and Outflow Vascular
Occlusion
Total HepaticVascular Exclusion (THVE)
Pringle maneuver is performed
Clamp across the infrahepatic IVC above the renal veins
Clamp across the suprahepatic IVC
 After completing the hepatectomy the clamps
are removed
Cross-clamping of the inferior vena cava and portal vein
 Venous return &cardiac output  40-60% decrease
 Systemic vascular resistance  80% increase
 Heart rate  50% increase compensatory
Unclamping
 Increase in cardiac index
 Reduction in systemic vascular resistance
 Requires volume loading to prevent profound
hypotension and potential cardiac arrest
 BeforeTHVE, colloids can be administered
Corrects volume defecit
Improves splanchnic circulation
Displace fluid into vascular space
Reduce bowel edema
Renal function preservation
 Perioperative fluid shifts,
 Intravascular hypovolemia, reduces RBF
 Sympathetic activation duringTHVE
Rx
 Mannitol
 Frusemide no evidence
 Low dose dopamine
 Hemodynamic intolerance toTHVE or
ischemia underTHVE exceeding 30 or 60
minutes, require venovenous Bypass
Selective Hepatic Vascular
Exclusion (SHVE).
 Continuous or intermittent manner
 Slight increase in systemic and pulmonary
resistance .
 Method of choice in cases when cvp cannot be
lowered(right heart failure, poor cardiovascular
status)
Vascular Air Embolism.
Factors predisposing
 (a) surgical technique,
 (b) size and place of the tumor,
 (c) blood loss, and
 (d) low CVP anesthesia.
Tumours
Right lobe
Close to IVC
Close to
cavo
hepatic jn
Cirrhotic patients have intrapulmonary shunting ,
pulmonary dilatation ,Arteriovenous communications
Paradoxical embolism can occur
Ischemia-Reperfusion Injury and
Preconditioning
 Ischemia/ reperfusion (I/R) injury 
causes a local and systemic inflammation
response
 Protective methods
Ischemic preconditioning
Intermittent clamping
Ischemic preconditioning
 Process in which a short period of ischemia, separated by
intermittent reperfusion, renders an organ more tolerant
to subsequent episodes of ischemia.
Post-operative concerns
 On table extubation
 Serum lactate measured
 Early increase in transaminases common
 Persistant increase ongoing hepatic ischemia
 Avoid hypothermia
 CVP measurement
CVP
 If patient is normotensive and urine output is
adequate (>0.5 mL/kg/hr), any attempt to
administer extra fluid to elevate CVP is
avoided especially in first 48 hours
Respiratory
 Atelectasis and subsequent pneumonia
 Basal collapse especially on the right
 Pleural effusion
 Failure to clear secretions and reexpand the
lungs  due to inadequate pain relief
Mx
 postoperative atelectasis should be treated
by early CPAP
 Early mobilisation
 DVT prophylaxis
Gastrointestinal
 Transient ascites
 Ileus
 rising liver enzymes in the 24-48 h after
surgery  liver ischemia
Renal System:
 Oliguria due to hypovolemia
Cardiovascular
 Arrythmias
 Hypotension
CNS
Drowsiness due to
 drugs
 hepatic encephalopathy
 Hypoglycemia
Check ammonia and glucose levels
Glycemic control
 Hyperglycemia due to surgical stress
 target range of 90-120 mg/dl
 Patients may develop insulin resistance
 Hypoglycemia due to impaired hepatic
mobilization of glucose
Nutrition
 post-hepatic resection period  catabolic
state
 High energy requirement by regenerating
liver
Coagulopathy
 Postoperative coagulopathy peaks 2-5 days
post surgery
 In non cirrhotics inc in PT INR is self limiting
 In cirrhotics FFP given
 Platelet transfusion if
plt count < 10000
plt count 10-30000 with active bleeding
 Peptic ulcer prophylaxis with a proton pump
inhibitor
 Regular nasogastric (NG) lactulose to prevent
gut stasis that contributes to encephalopathy
Pain management
 Epidural analgesia
 Opioids
 Patient controlled analgesia (PCA)
 NSAIDs is not recommended
 Preoperative american society of
anesthesiologists (ASA) classification
 Steatosis
 Extent of resection
 Simultaneous extrahepatic resection,
 Perioperative blood transfusion
have been found to be independent predictors for
the development of postoperative complications
References
 Miller 8th edition
 Anaesthesia for hepatic resection surgery
Continuing Education in Anaesthesia,CriticalCare & Pain |Volume 9
Number 1 2009 &The Board of Management andTrustees of the
British Journal of Anaesthesia
 Epidural anaesthesia and analgesia for liver resection
Anaesthesia © 2013The Association of Anaesthetists of Great Britain
and Ireland
 Perioperative management of hepatic resection
Journal of GastrointestinalOncology,Vol 3, No 1, March 2012
Thank you

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Hepatectomy anaesthesia

  • 1. ANESTHESIA FOR LIVER RESECTION Dr Kiran Rajagopal DA DNB Anaesthesiologist
  • 2. Indications  Removal of hepatic metastases from colorectal carcinoma  Removal of primary hepatic tumours such as hepatocellular carcinomas or biliary tumours such as cholangiocarcinomas  Following trauma to the liver.  Removal of benign liver tumours(hepatic adenoma), liver cysts  Live donor liver transplantation.  Segmental resections may be required as part of hepaticojejunostomy procedures for high bile duct injuries
  • 3. Laparoscopic hepatectomy  Far less common than open procedures  Recognized for  liver cysts  peripheral solitary metastases  hepatocellular carcinoma.
  • 5.  Access: incision is upper midline, extending to right subcostal region (Lexus incision).  Mobilization: division of the triangular ligaments (frees the liver from the diaphragm). Mobilization of the vena cava. cholecystectomy done  Inflow control: obtained by a variety of techniques (eg. dissection of the liver hilum with control of the portal vein and hepatic artery, dividing the bile duct within the liver substance. Or, alternatively, dissection of the intrahepatic inflow pedicle etc)  Outflow control: classically, the hepatic vein is divided extrahepatically, but can also be divided within the liver during parenchymal transection.
  • 6.  Parenchymal resection:  Before resection,CT and MRI to confirm exact tumour location and vascular anatomy Intra-operative ultrasound is mandatory to confirm preoperative assessments and identify additional lesion  Parenchymal transection has been described using a number of techniques. Commonly, dissection with a clamp crushing technique or Cavitron Ultrasonic Aspirator (CUSA) are used to disrupt liver parenchyma, revealing vessels and bile ducts that may then be clipped or ligated.
  • 7.  Confirmation of haemostasis and abdominal closure Haemostasis achieved with the use of argon beam coagulation and fibrin glues
  • 8. Recently the trend has moved away from “anatomical resection” (respects the portal triad) towards “non-anatomic resection” (resection of a lesion with 1-2 cm margins, irrespective of hepatic anatomy).
  • 10. Pre operative  Preoperative assessment should be adapted to the needs of each individual patient, based on general comorbidities and hepatic function.  Patients without parenchymal liver disease are assessed as for any major intra-abdominal operation.  Patients with hepatic disease are at significantly increased risk of multi-organ dysfunction, including cardiac failure, impaired gas exchange, bleeding and renal failure
  • 11. Colorectal metastasis  neo-adjuvant chemotherapy  5-Fluorouracil (5-FU) with leucovorin and oxaliplatin Pros Cons Neo adjuant chemotherapy
  • 12. Pre operative  Of particular concern are conditions causing an elevation of right-side cardiac and central venous pressure (CVP) that significantly increases the risk of intra-operative bleeding.  Early communication with the surgical team will identify cases with a high risk of intra-operative bleeding, large resection, or postoperative liver failure
  • 13. Assessment of liver function  In young patients with normal hepatic parenchyma, it is safe to remove up to four liver segments amounting to a 50–60% resection  survival after 80% resection is possible.  postoperative liver failure can occur  underlying chronic liver disease presenting for liver resection are at high risk of postoperative liver failure
  • 14. Child-Pugh scoring  Child B &C unfit for liver resection  indocyanine green (ICG) retention- measures liver perfusion and biliary excretion  Impaired clearance of ICG is suggested when more than 15% of the dose remains in the plasma 15 min after injection
  • 15. Predictors of transfusion  a) preoperative hemoglobin concentrations below 12.5 g/dl,  (b) tumor more than 4 cm,  (c) need for exposure of the vena cava,  (d) need for an associated procedure, and  (e) cirrhosis
  • 16. Intraoperative  GA ,ETT ,CV with or without thoracic epidural  Little evidence to favour any particular choice of anaesthetic agent  Hepatic clearance will be reduced after resection  Known hepatotoxins such as halothane avoided  Nitrous oxide should be avoided as it causes gut distension and there is a small risk of air embolism
  • 17. EPIDURAL Benefits Risks  Post op analgesia  Less pulmonary complications  Sympathetic blockade - low CVP reduces blood loss and transfusion requirements  Post op coagulopathy  Pre op coagulopathy  Epidural hematoma/abscess  Increased total intravenous fluid administration  Increased transfusion due to haemodilution Even in patients with pre op normal liver function and coagulation, prothrombin time (PT) is prolonged in the majority of patients on the first and second postoperative days and may remain abnormal for up to 5 days
  • 18. Monitoring  Minimum monitoring standards  Invasive arterial and CVP  Blood glucose monitoring  Naso-gastric tube  Temperature monitoring – warmer  Neuro muscular monitoring Large bore intra-venous access A rapid infusion system should be available
  • 19. Blood Loss  Blood loss of 10 litres has been reported after liver resection  Large transfusions are a risk factor for major postoperative complications and liver failure.  Patients with cirrhosis, steatosis, and after chemotherapy are at especially increased risk of coagulopathy and bleeding
  • 20. TECHNIQUES TO LIMIT BLOOD LOSS
  • 21. Pringle maneuver  A noncrushing clamp or a tourniquet is placed around the structures in the porta hepatis to occlude portal venous and hepatic arterial inflow during parenchymal transection.  Intermittent or continuous  Occlusion time limited to an hour or less  Reduce the blood loss by up to approximately 65%
  • 22. CVS Effects  MAP increase by 6%  Cardiac output decrease by 10%  Left ventricular afterload increase of 20–30%  Hypotension after clamp release
  • 23. Hepatic vascular control methods 1) Inflow vascular occlusion (A) Hepatic pedicle occlusion: (a) Continuous Pringle maneuver (CPM) (b) intermittent Pringle maneuver (IPM) (B) Selective inflow occlusion. (2) Inflow and outflow vascular exclusion (A) Total hepatic vascular exclusion (THVE) (B) Inflow occlusion with extraparenchymal control of the major hepatic veins: with selective hepatic vascular exclusion (SHVE).
  • 24. Inflow Vascular Occlusion  CPM, IPM, and selective inflow occlusion - same haemodynamic management  Portal triad clamping - increases systematic vascular resistance reduces cardiac output increases Mean arterial pressure  On unclamping - parameters return to baseline values.  Main source of bleeding is backflow from the valveless hepatic veins
  • 25. Low CVP  CVP (between 2 and 5 mmHg) -- reduces blood loss  Limit iv fluids  Diuretics or Nitrate infusion  Nitroglycerin reduces CVP to the desired level during the resection phase or when excessive oozing is observed from the resected surface.  After the resection – restore circulating blood volume
  • 26.  PEEP increases CVP & reduce liver blood flow  Avoid PEEP during resection phase  15◦ Trendelenburg position can be given -- prevents air embolism
  • 27. Risks of low CVP  Cardiovascular instability  Air embolism  Postoperative renal dysfunction If urine output falls to 0.5 ml/ kg/ h or Refractory hypotension occurs  small colloid bouses may be given
  • 28. Inflow and Outflow Vascular Occlusion Total HepaticVascular Exclusion (THVE) Pringle maneuver is performed Clamp across the infrahepatic IVC above the renal veins Clamp across the suprahepatic IVC  After completing the hepatectomy the clamps are removed
  • 29. Cross-clamping of the inferior vena cava and portal vein  Venous return &cardiac output  40-60% decrease  Systemic vascular resistance  80% increase  Heart rate  50% increase compensatory Unclamping  Increase in cardiac index  Reduction in systemic vascular resistance
  • 30.  Requires volume loading to prevent profound hypotension and potential cardiac arrest  BeforeTHVE, colloids can be administered Corrects volume defecit Improves splanchnic circulation Displace fluid into vascular space Reduce bowel edema
  • 31. Renal function preservation  Perioperative fluid shifts,  Intravascular hypovolemia, reduces RBF  Sympathetic activation duringTHVE Rx  Mannitol  Frusemide no evidence  Low dose dopamine
  • 32.  Hemodynamic intolerance toTHVE or ischemia underTHVE exceeding 30 or 60 minutes, require venovenous Bypass
  • 33. Selective Hepatic Vascular Exclusion (SHVE).  Continuous or intermittent manner  Slight increase in systemic and pulmonary resistance .  Method of choice in cases when cvp cannot be lowered(right heart failure, poor cardiovascular status)
  • 34. Vascular Air Embolism. Factors predisposing  (a) surgical technique,  (b) size and place of the tumor,  (c) blood loss, and  (d) low CVP anesthesia. Tumours Right lobe Close to IVC Close to cavo hepatic jn Cirrhotic patients have intrapulmonary shunting , pulmonary dilatation ,Arteriovenous communications Paradoxical embolism can occur
  • 35. Ischemia-Reperfusion Injury and Preconditioning  Ischemia/ reperfusion (I/R) injury  causes a local and systemic inflammation response  Protective methods Ischemic preconditioning Intermittent clamping
  • 36. Ischemic preconditioning  Process in which a short period of ischemia, separated by intermittent reperfusion, renders an organ more tolerant to subsequent episodes of ischemia.
  • 37. Post-operative concerns  On table extubation  Serum lactate measured  Early increase in transaminases common  Persistant increase ongoing hepatic ischemia  Avoid hypothermia  CVP measurement
  • 38. CVP  If patient is normotensive and urine output is adequate (>0.5 mL/kg/hr), any attempt to administer extra fluid to elevate CVP is avoided especially in first 48 hours
  • 39. Respiratory  Atelectasis and subsequent pneumonia  Basal collapse especially on the right  Pleural effusion  Failure to clear secretions and reexpand the lungs  due to inadequate pain relief
  • 40. Mx  postoperative atelectasis should be treated by early CPAP  Early mobilisation  DVT prophylaxis
  • 41. Gastrointestinal  Transient ascites  Ileus  rising liver enzymes in the 24-48 h after surgery  liver ischemia
  • 42. Renal System:  Oliguria due to hypovolemia
  • 44. CNS Drowsiness due to  drugs  hepatic encephalopathy  Hypoglycemia Check ammonia and glucose levels
  • 45. Glycemic control  Hyperglycemia due to surgical stress  target range of 90-120 mg/dl  Patients may develop insulin resistance  Hypoglycemia due to impaired hepatic mobilization of glucose
  • 46. Nutrition  post-hepatic resection period  catabolic state  High energy requirement by regenerating liver
  • 47. Coagulopathy  Postoperative coagulopathy peaks 2-5 days post surgery  In non cirrhotics inc in PT INR is self limiting  In cirrhotics FFP given  Platelet transfusion if plt count < 10000 plt count 10-30000 with active bleeding
  • 48.  Peptic ulcer prophylaxis with a proton pump inhibitor  Regular nasogastric (NG) lactulose to prevent gut stasis that contributes to encephalopathy
  • 49. Pain management  Epidural analgesia  Opioids  Patient controlled analgesia (PCA)  NSAIDs is not recommended
  • 50.  Preoperative american society of anesthesiologists (ASA) classification  Steatosis  Extent of resection  Simultaneous extrahepatic resection,  Perioperative blood transfusion have been found to be independent predictors for the development of postoperative complications
  • 51. References  Miller 8th edition  Anaesthesia for hepatic resection surgery Continuing Education in Anaesthesia,CriticalCare & Pain |Volume 9 Number 1 2009 &The Board of Management andTrustees of the British Journal of Anaesthesia  Epidural anaesthesia and analgesia for liver resection Anaesthesia © 2013The Association of Anaesthetists of Great Britain and Ireland  Perioperative management of hepatic resection Journal of GastrointestinalOncology,Vol 3, No 1, March 2012