ANAESTHETIC MANAGEMENT

IN LIVER TRANSPLANT
 HISTORY
•1963 first human liver transplant by starzl et al
(orthotropic liver transplantation)

•1967 first long survival

•1979 Cyclosporine – Sir Roy Calne

•1987 UWI solution for improved organ preservation

•1999 Living Donor liver transplantation
 INTRODUCTION
 Liver transplant is the sole life saving procedure for
the patients with end stage liver disease (ESLD)

 Major goals of liver transplantation are :-

 To prolong survival

 To improve quality of life

 Improvements in organ preservation, surgical

technique, better Immuno suppressive agents,
management of coagulopathy and treatment of
infections has resulted in great expansion of this
procedure
 LIVER DONOR
•Deceased (brain dead) donor liver transplantation (DDLT)

•Living Donor liver transplantation (LDLT)

- Based on concept that liver has high regenerative capacity

- In adult to adult LDLT, larger right lobe of donor is used

(segment V, VI, VII & VIII)

- Graft size 500 – 1000gm, donor is left with 1/3rd of original mass

- In children only left little segment (II & III) or entire left lobe (II, III,
IV) can be used depending on the weight of the recipient

- Left hepatectomy is less complex and require less surgical time.

 LIVER DONOR
Advantages of LDLT
• Hemodynamic stability of donor – better graft
quality
• Reduced cold Ischemia time
• Reduced waiting time
• Elective nature of procedure permitting optimal
preparation of recipient
Problems of LDLT
• Donor morbidity
• High incidence of hepatic artery thrombosis
 LIVER DONOR
Split grafts
• Limited availability of suitably sized pediatric livers had
lead to development of split grafts in which a single
organ donor may be splitted for multiple transplant

Problems
- More complications
- Excessive bleeding and tissue necrosis
- Reduced survival rate in recipients
- High incidence of hepatic artery thrombosis
 INDICATIONS
Adults
• Chronic hepatitis
• Chronic hepatitis B
• Cryptogenic cirrhosis
• Hepato-cellular carcinoma
• Alcoholic liver disease
• Fulminant hepatic failure
• Wilson’s Disease
• Primary biliary Cirrhosis
• Metabolic and genetic disorders
 CONTRAINDICATIONS
Absolute contraindications
• Extra hepatic malignancy
• Active sepsis
• Advanced cardiac disease
• Advanced pulmonary disease
• HIV with AIDS and low CD4 counts

Relative Contraindications
• Advanced chronic renal failure
• Psychological factors like active alcohol and drug abuse
• Hypoxemia with intra pulmonary Rt to Lt shunt
• Portal Vein thrombosis
 SCORING SYSTEM
Childs –Turcotte-Pugh (CTP)
classification
Childs –Turcotte-Pugh score 1 point 2 points 3 points
Characteristics
Ascites None Controlled Refractory
Encephalopathy Absent Grade 1-2 Grade 3-4
Albumin (mg/dL) >35 28-35 <28
Bilirubin (mg/dL) <2 2-3 >3
INR <1.7 1.7-2.3 >2.3

Points Class Life expectancy Perioperative

mortality
5-6 A 15-20 years 10%
7-9 B Candidate for transplant 30%
10-15 C 1-3 months 82%
DRAWBACKS

• Ascites and encephalopathy, are subjective as

assessed by physical examination alone

• When other methods are used (USG, EEG,

Psychiatric evaluation) a different degree of severity
is diagnosed

• Renal function assessment is absent – well

established prognostic marker in cirrhosis.
 MODEL FOR END STAGE LIVER DISEASE (MELD)
• It is a mathematical formula based on following factors
 Creatinine (for adult pts undergoing dialysis twice a week within
the last week, the Creatinine value would be automatically set to
4mg/dL)

 Bilirubin

 International normalised ratio

MELD score formula

MELD score = (0.957 x loge[serum Creatinine(mg/dL)] + 0.387 x

loge[total serum bilirubin (mg/dL)] 1.120xloge[INR])x10

- Score tells how urgently Liver Transplant is required &

mortality within next 3 months

- Most pts on Liver Transplant waiting list have MELD score

between 11 & 20
Goal oriented anaesthetic management require the
understanding of following:-

 Pharmacokinetics & Pharmacodynamics

 Patho-physiology of liver failure

 Physiology of vascular exclusion

 Physiology of surgical resection

 COMMON INVESTIGATIONS
• Complete Haemogram – to establish anemia, thrombocytopenia or
evidence of infection

• Pro-thrombin time – raised due to vitamin K def

• Baseline renal function – Creatinine may indeed represent renal

impairment
• Serum Electrolytes

• ECG & 2D Echo – to establish ventricular function, presence of

cardiomyopathy, valvular lesions, raised pulmonary vascular pressure

• Stress Echo – In chronic state, vasodilatation may mask ischemia by

limiting ventricular workload, stress testing may be useful where
undiagnosed ischemia is suspected

• CXR and PFT

• ABG
 BLOOD PRODUCTS
• 10 U of Red Blood Cells

• 10 U Fresh Frozen Plasma

• 4 U of Single donor platelets

• 10 U of Cryoprecipitate
 PREPARATION OF OT
• Warm Room to 21 – 26 degree Celsius (Paediatric Cases)

• Fluid warming devices, Airway Humidifier & Forced air

warming device (e.g. Bair Hugger)

• Rapid fluid infusion systems, including pressurized devices

• Availability of blood and blood components in OT & Blood

salvaging devices eg: cell saver

Drugs : Antibiotics, ionotropes, vasopressors, electrolytes,

dextrose, insulin, lignocaine, albumin

Monitoring : trans-esophageal echocardiography, invasive

hemodynamic monitoring, NM Monitoring
INDUCTION OF ANAESTHESIA
• Opioids: Fentanyl

• Induction agent: Propofol, thiopental, or etomidate

• Muscle relaxant: SCh (plasma pseudo cholinesterase levels

decrease in liver disease, resultant prolongation of SCh effect,
caution : K level )

. RSI : delayed gastric emptying, gross ascites, active GI bleeding or

encephalopathy

• NG tube - improve surgical exposure, early enteral feeding

-Chances of bleeding during NG insertion

• Post induction hypotension

- Very low SVR & Relative hypovolemia
- Correction by small amount of vasoconstrictors
 MAINTENANCE OF ANAESTHESIA

• Nitrous oxide : Intestinal distension, hence avoided

• Balanced anesthesia technique with volatile anesthetics in

oxygen/air mixture and opioids provide stable hemodynamics

• Isoflurane commonly used (splanchnic vasodilator

properties, HABF preserved by preservation of auto regulation)

• Muscle relaxant : Cisatracurium or Atracurium preferred

over Vecoronium

• Neuro Muscular monitoring recommended

INTRA-OPERATIVE KEY ISSUES
 Major bleeding

 Coagulopathy

 Electrolyte disturbances

 Hemodynamic instability
INTRAOPERATIVE MONITORING
 Centre specific
 Patient specific
 Minimum Mandatory Monitoring: ASA standard for Basic
Anaesthesia Monitoring
 IBP, Epidural
 CVP in all pts / Pulmonary artery catheter (in selected
cases)
 CO Monitoring LiDCO / FloTRAC
 Trans-oesophageal echocardiography (TEE)
 VASCULAR ACCESS
 Unpredictable blood loss :
 H/o Previous upper abdominal surgery
 Highly coagulopathy condition

 Significant portal HTN

 CVC - two : one large bore for rapid infusions and other one 3/4
lumen for drug administration

 Internal jugular vein (preferably right side) is the selected route for
cannulation.

 Correction of coagulopathy before line placement

 Sites designated for Veno venous bypass should be avoided.

 PRESSURE POINT CARE
- Lower limbs (knee & ankle)- boots
- Upper limbs – apply gel pads, silicon pads
- Head- Gel ring
 FLUID BALANCE
 5% Dextrose is started from beginning to prevent

hypoglycemia.

 Other crystalloid used is Plasmalyte A (pH corrected

crystalloid having pH 7.4).

 IV volume is maintained by
› Albumin,

› 6% HES/Gelfusion,

› Blood & Blood products as indicated by Hct and TEG

 INTRA-OPERATIVE GOALS

 Hb 8-9gm/dl
 Normothermia
 Electrolyte and acid base balance
 MAP≥60 mm of Hg and SVV≤10
 Urine output at least 0.5 ml/kg/hr
PHASES OF LIVER TRANSPLANT SURGERY

 Dissection phase

 An-hepatic phase

 Reperfusion phase (Neo-hepatic phase)

 STAGES OF OPERATION IN LIVER TRANSPLANTATION

Pre-an-hepatic/
Neo-hepatic /
An-hepatic phase
dissection phase Reperfusion phase

Dissection of Begins when native liver is Completion of

structures of porta removed after transaction of anastomoses,
hepatis & blood supply & occlusion of hemostasis, graft
skeletonization of supra- and infra- hepatic IVC reperfusion, biliary
native liver & implantation of donor liver drainage and
closure.
 INCISION

Inverse T or Mercedes incision

 DISSECTION PHASE
(KEY ISSUES)
 Intra-vascular volume depletion
 Blood loss
 Caval handling
 Ascitic fluid drainage
 Translocation of bacteria
 Adhesions/SBP
 Portal vein clamping (temporary)
 Air embolism
 Hypothermia
 Decrease urine output
 Electrolyte and Acid Base disturbances
 DISSECTION PHASE
(MANAGEMENT)

 Crystalloids & Colloids : CVP & SVV guided

 Blood & Blood products : TEG guided

 Correction of Acidosis & Dyselectrolytemia as per ABG

 DISSECTION PHASE (MANAGEMENT)

 Look for signs of septicemia

- ↓SVR

- ↓ABP

- ↑Lactate

 Consider up-gradation of antibiotic if unresponsive to

vasopressors and fluids
 Maintain normoglycemia & normothermia
 DISSECTION PHASE (MANAGEMENT)
Electrolyte disturbances
 Hyponatremia:
 Dilution Hyponatremia

 Should not be corrected rapidly.

 Should be maintained closer to preoperative.

 Not to be increased by more than 10-12 mmol/l in 24 hrs to prevent cerebro-

pontine myelinosis

 Hypocalcaemia:
 Due to citrate intoxication resulting from infusion of blood products in absence of

liver function
 Avoided by administration of calcium chloride
 Hypomagnesaemia:
 Results from citrate infusion

 Magnesium 2gm infusion

 Value usually comes to normal after graft reperfusion.

 Hypokalemia:
 Avoid aggressive treatment of Hypokalemia.
 ANHEPATIC PHASE

 New liver is implanted by one of the two

techniques

- Intra-Caval interposition

- Piggy-back technique
 INFRA –CAVAL INTERPOSITION
(VENO VENOUS BYPASS)

 Complete vascular occlusion by

clamping hepatic artery, portal
vein, supra and infra hepatic IVC

 Decreases venous return around

50%
 Diverts IVC and portal venous flow
to axiliary vein
 Attenuates decrease in preload,
improves renal perfusion pressure,
attenuates splanchnic congestion,
and delays the development of
metabolic acidosis
 PIGGY-BACK TECHNIQUE

 Allows removal of liver without

removing the portion of vena cava

 One end of donor IVC is closed

and other end is anastamosed to
recipient IVC end to side

 Temporary Porto caval shunt is

performed to reduce the portal
pressure

 Adv : Improved hemodynamic

 Disadv : Surgically more difficult
than caval
 ANHEPATIC PHASE
 Starts from clamping of portal vein

 Increase in portal pressure results in bowel congestion and may

increase surgical bleeding.

 Physiological changes are caused by removal of liver.

 IVC cross clamping → CO ↓ (Marked in HCC patient with absence of

collaterals)
 IVC side clamping is done if Patient dose not tolerate cross clamp or
pre-op renal dysfunction.
 Removal of native liver → O₂ consumption↓ → CO ↓
 ANHEPATIC PHASE
 Fibrinolysis can occur as the tissue plasminogen activator not
being removed from circulation and absence of liver produced
plasminogen activator inhibitor.
 Absence of liver → Inability to metabolise Citrate → Citrate toxicity
→ Presents with ↓Ca²⁺ & myocardial depression.
 Hypocalcaemia must be corrected before reperfusion

 Some patients who were unstable in dissection phase start

stabilizing because the liver which was producing vasoactive
substances is now out of circulation.
ANHEPATIC PHASE (KEY ISSUES)

 Worsening Coagulopathy
 Hypothermia
 Hypoglycemia
 Hypocalcaemia
 Acidosis
 ↑ Lactate
 ↓ Urine output
ANHEPATIC PHASE (MANAGEMENT)

IVC CLAMPING TYPES


Test clamp

Total clamp

Side clamp
 ANHEPATIC PHASE (MANAGEMENT)
Test IVC Clamping


To be done for 01 min to see the hemodynamic effects.


There will be expected drop in CO.


It can be managed with vasopressors and volume adjustments.

If systolic pressure falls to less than 70% of its previous value
(SAP<80-90 MM OF Hg or MAP<60 mm of Hg) in the presence of
adequate blood/fluid placement, bypass support may be needed or
surgical plan is modified to avoid total vascular exclusion.
IVC CROSS CLAMPING
 Before IVC clamping

 Adequate volume expansion

 Mannitol 20% IV bolus (0.3-0.5 g/kg)

 Methylprednisolone 10 mg/kg

 During IVC clamping

 Ionotropic support

 Strict volume adjustment to avoid overload.

 If MAP drops still precipitously in spite of vasopressor support and fluid
loading, unclamping should be done and alternate mode of circulatory
support must be considered.
MAINTENANCE OF RENAL FUNCTION

 Urine output is decreased during cross clamping.

 Renal function is maintained by:

 Mannitol - osmotic diuretic, free radical scavenger, antioxidant,
removes free water within congested abdominal organs, prevents
hepatic distension
 Intravenous fluids

 Vasopressors

 Renal dose of dopamine

 Side clamping

 Veno-venous bypass
 BEFORE UNCLAMPING
 Getting ready for Reperfusion
 Normalize serum electrolytes; keep calcium 1-1.2 mmol/ltr and potassium

4 mmol/ltr

 Keep body temp >36◦C

 Blood and colloids ready for rapid infusion (pressure bags on)

 Correct acidosis/coagulopathy/Hb before reperfusion

 Adrenaline available as 100µg/ml & 10 µg/ml

 Heparin 4000 units in anhepatic phase + 4000 units after reperfusion in

patients with HbsAg positive status.

 Keep ready Atropine , Lasix, Calcium and NaHCO3.

 NEOHEPATIC / REPERFUSION PHASE
(DESIRED EFFECT)
Hemodynamic stability
- MAP 60 – 90 mmHg
- CVP < 10 cm of H2O
 Look for good graft function
- Correction/absence of acidosis
- Adequate urine output
- Normalizing/decreasing lactate levels
- Hyperglycemia
- Non congested graft
- Temp stabilization
 REPERFUSION PHASE

 Changes due to Ischemia reperfusion injury

 Minimized by giving Methyl pred10mg/kg before reperfusion

 Release of vasoactive substances from Ischemic liver graft

& from static blood from gut → sudden ↓ in HR, MAP, SVR.

 Treatment of hypotension is with vasopressors like nor

adrenaline.
 REPERFUSION PHASE
 Sudden ↑ in Serum K⁺ levels which can be offset by
giving Ca²⁺ bolus.

 Worsening of metabolic acidosis due to sudden

reperfusion of ischemic liver and obstructed splanchnic
bed.
 NEOHEPATIC PHASE

 Hepatic Artery Anastomosis

 Ultrasound Doppler

 Biliary Anastomosis

 Haemostasis

 Wound Closure
POST-REPERFUSION SYNDROME
 Drop in blood pressure of more than 30% from baseline,
lasting for 1 min or more and occurs within 5 mins after
reperfusion.

 Etiology:-
 Due to release of metabolites from graft and congested intestines.

 Hyperkalemia

 Acidosis

 Hypothermia

 Air or thrombotic emboli

POST-REPERFUSION SYNDROME

 Management:-

 Continuous monitoring of ECG, BP, SV, SVV, CO.

 Start nor adrenaline infusion if required

 Blood and colloids infusion ready for rapid infusion

 Calcium chloride to counter potassium load

 Sodium bicarbonate to counter acidosis

 Adrenaline available.
 SPECIFIC COMPLICATIONS
 Initial poor graft function
 Persistence of metabolic acidosis
 Continued hemodynamic instability
 Congested or grayish appearance of liver
 Coagulopathy
 Low urine output
 Hypotension

Management:
 Continued use of N-acetylcysteine
 Nor adrenaline
 Air embolism
 During dissection phase

 When graft gets back into circulation.

 More likely to happen if the venous pressure is low.

 Diagnosed by fall in ETCO2 and adverse hemodynamic events.

 Thrombo-embolism
 During reperfusion phase

 From veno-venous bypass circuit

 LOW CVP STRATEGY
 Reduce the blood loss by preventing the distension of
hepatic veins and sinusoids.

 Reduce blood and blood products transfusion

requirements.

 Improve oxygen delivery to donor graft.

 Creates a venous gradient between portal and central

venous circulation that draws blood through the donor
graft.
 PAIN MANAGEMENT
 Most patients remain intubated :- receive potent opioids
as sedatives.

 LTx patients has less post op pain than hepatectomy :-

 Difference in pain threshold , reason – unclear

 Elevation of neuropeptide metenkephalin which is

involved in pain modulation.

 Steroids :- used for Immuno-suppresion

 POST-OPERATIVE CARE
• Ventilator support for 6-12 hours
• Sedation and analgesia (propofol and fentanyl)
• Tight glycemic control
• Coagulation and full blood count , Hematocrit between 24-30 hours
• Immuno suppression at the earliest
- Triple therapy
 Calcineurin Inhibitor (tacrolimus, cyclosporine)
 Anti proliferative agent (Mycophenolate)
 Corticosteroid
• Frequent Doppler assessment of the graft
EXTUBATION
 POST-OP MANAGEMENT
• Hemodynamic support

• Ventilator support

• Metabolic

• Hemostatsis

• Renal

• Prevention of infections

• Early nutrition therapy

 POST-OPERATIVE COMPLICATIONS

• Primary non function (5%)

• Rt Pleural effusion
• Hemorrhage
• Renal Failure
• Electrolyte imbalance
• Thrombocytopenia
• Billiary leak
• Hepatic artery thrombosis