LIVER TRANSPLANT

ANAESTHETIC MANAGEMENT
BY
DR SAMEER
DR SHALVI
DR ASHOK
DR SHANMUGAM
INDICATIONS OF LIVER TX
1. END STAGE LIVER DISEASE 4. FULMINANT HEPATIC
 ALCOHOLIC, FAILURE
 DRUG INDUCED
 VIRAL MOSTLY HEP C
 ACUTE VIRAL HEPATITIS
 CHRONIC DRUG INDUCED
5.METABOLIC DISORDERS
2. CHOLESTATIC
 α1-ANTITRYPSIN DEFICIENCY
 PSC
 WILSONS DISEASE
 PBC
 HEMOCHROMATOSIS
 BILIARY ATRESIA
6.MALIGNENCIES NOT
3. VASCULAR DISEASES AMENABLE TO THERAPY
 BUDD CHIARI SYNDROME
 HCC
 VENO OCCLUSIVE  CHOLANGIOCARCINOMA
 POLYCYSTIC LIVER DISEASE  CARCINOID
Contraindications to
Liver Transplantation
ABSOLUTE RELATIVE
 BRAIN DEAD  OBESITY
 BACTERIAL PERITONITIS  MOD PAH, MOD AS
 METASTATIC HB TUMORS  CRF
 AIDS  HYPONATREMIA
 ADVANCED CADIAC  PORTAL VEIN
DISEASE THROMBOSIS
 UNTREATED CAD  HEPATIC COMA WITH ↑ICP
 CRITICAL AS  ACTIVE ALCOHOL ABUSE
 RECENT DRUG ELUDING  ADVANCED AGE
STENT  MALNUTRITION
 SEV PAH  POOR ECONOMIC STATUS
Most common indication is alcoholic liver disease.
Patients with fulminant hepatic failure require particular
attention-infections are common
Incipient brain herniation is commonly assessed by serial
head CT or, ideally, by ICP monitoring.
Patient selection-comply life style
alcohol drug abstinence
lifelongimmunosupressants
Liver transplant listing committee-surgeons and
hepatologists, anesthesiologists,psychiatrists,addictions
specialists, social services specialists, family therapists
and financial assistance experts
MELD Scoring System
priority ranked by application of the Model of End-
Stage Liver Disease (MELD) scoring system. 6-40.
analogous system for pediatric patients, the PELD
scoring system, is applied for ≤12 years. Has
bilirubin,age,INR,albumin,growth failure.
MELD scoring system uses a multivariate regression
model to calculate risk of death from the patient’s liver
disease based on prognostic factors
MELD Score = (0.957 × loge[creatinine mg/dL] + 0.378 ×
loge[bilirubin mg/dL] + 1.120 ×loge[INR] + 0.643) * 10
Lower limit is 1 for all variables
Max creat value is 4.for HD patients 4.
Exceptions- 1A
1. Fulminant hepatic failure
2. Life expect less than 7days without liver tx
3. Nonfunctioning or hepatic.a thrombosis in graft within
7days of tx
4. Acute decompensated wilsons disease
 ORGAN PRESERVATION
Cold storage and perfusate
Principle: hypothermia reduces the metabolism and
enzymatic activity and slows down cell death, but during
the process it causes cellular oedema
Euro Collins,UW,HTK,Marshall’s hypertonic citrate.
UW and HTK most common
UW being expensive with increased viscosity and a high
potassium/low sodium ratio (120 mM/L, 25 mM/L)
HTK is inexpensive, less viscous and has a low
potassium/high sodium ratio (9 and 15 mM/L)
Machine perfusion
Hypothermic machine perfusion (HMP) combines
hypothermia and perfusion to restoration of energy and
oxygenation
used in renal and in lung transplantation
Ischemia reperfusion injury
microcirculatory failure, production of reactive oxygen
species, inflammatory responses and apoptosis of the
hepatocytes
N-acetyl cysteine (NAC) is being used to prevent renal
failure and prevent IRI of new liver
Preanesthetic Evaluation
most patients are “well studied”
hepatic synthetic function-serum albumin and bilirubin
Coggulation-prothrombin time, partial thromboplastin time,
fibrinogen
platelet count-decrease due to splenic sequestration,uremia
Neurologic status-
Raised icp-treat triggers,oral lactulose,
antibiotics(rifaximin,neomycin,vancomycin,metronidazole)
,mannitol
reassess
cardiac risk during the history
Serum electrolytes-hyponatremia,hypokalemia or
hyperkalemia, hypocalcemia, and hypomagnesemia.
physical examination- Ascitis- regurgitation and
aspiration, compromises pulmonary performance, rapid
and severe desaturation.
Ascitis-low sodium diet,albumin
replacement,paracentesis(risk factor for HRS)
look for large bore I.V access 14g, above diaphragm
Transjugular intrahepatic portosystemic shunt
bridge to liver tx from ESLD.
Treat hyponatremia-hypo or hypervolemic
 Diagnostic Studies
Hemoglobin,electrocardiogram,chest x ray
Platelet count
hepatic synthetic and excretory function
serum albumin and bilirubin
Routine coagulation studies
Serum electrolytes is essential to provide baseline data
BUN and creatinine-intraoperative renal replacement therapy
arterial blood gas measurement-hypoxia,indicate HPS
pulmonary function testing-small lung volumes(ascitis)
Cardiac assessment-CAD of grave concern,therapy is difficult
History of coronary disease
or congestive heart failure
• Signs or symptoms of
coronary disease or
congestive heart failure
• Abnormal ECG
• Diabetes
• Current or prior smoking
• Hypertension
• Hyperlipidemia
• Obesity
• Age > 50 for males, > 55
for females even in absence
of any of the above
Diagnostic Studies
hypothetical state with heart rate >110 beats/min, mean
arterial pressure <50 mm Hg, hemoglobin 7 g/dL, and pH
<7.2.
Dobutamine stress echocardiography-best screening test
cirrhotic cardiomyopathy-supranormal cardiac outputs
causes-impaired βadrenergic system
-excess NO production,cytokines
-prolonged hyperdynamic state
screening transthoracic echocardiogram-PPH,structural-
valvular,ASD
evaluating portopulmonary htn-
Pre Operative preparation for recipient

 Pleural effusion drained.

 Deranged coagulation profile – treated.
 Electrolyte imbalance corrected.
 Infection / sepsis corrected.
 Haemo / peritoneal dialysis, if required
 Blood products –
 10 U of red blood cells ,
 10 U of fresh frozen plasma
 4 U of single-donor platelets.
Anesthesia for liver recipient

Premedication:
 Abnormal coagulation –IM premedication usually

avoided.
 Hepatic encephalopathy -contraindication.

 If coagulation & level of consciousness are normal

premedication is not a contraindication.

 Dose is adjusted downward - reduced hepatic function
Operative Approaches
1. Hepatic resection
Two different techniques are commonly used for
controlling hepatic venous outflow and constructing
the hepatic venous anastomosis
(1) en bloc (2) a “piggyback” technique
Enblolc: recipient’s vena cava is resected and replaced
with a section of the donor vena cava
Piggyback-“side-biter” clamp placed on the inferior
vena cava isolates the liver from the systemic venous
system
Enbloc technique
1.severe reduction in venous return
2.below the caval cross-clamp venous congestion and
ischemia
3. profound hemodynamic instability
Caval clamping response - “test clamp”
Complications are avoided using venovenous bypass
Declamping -volume overload
right heart dysfunction
Hemodynamic instability depends upon - cardiovascular
reserve and extent of collaterals
 Piggy back technique
The venacava deep to side biter clamp is largely open
to flow
Allows lower systemic venous return,but not portal
the piggyback technique may take longer to perform.
lower incidence of renal failure
better gas exchange,
Better acid–base status at reperfusion,
intraoperative hemodynamic stability
Decresed need for transfusion, inotrope use
Disadvantage-portal congestion
 Venovenous bypass
First described in 1984
used to decompress the lower systemic venous
circulation, the portal circulation
Caval clamp → ↓venous return→ fall in CO →fall in
bp
↓ ↓
venous congestion dec organ
perfusion
↓
renal venous congestion and renal failure
Specific indications of VVBP :
1.pre-existing cardiac disease
2.severe PHT
3.hemodynamic instability
4. anaesthesiologist’s unfamiliarity with the technique
Drainage site for lower systemic circulation-ltfemoral
or portal vein.
Common return sites are the right internal jugular and
left internal jugular and lt subclavian veins
Flow-1.5-5 lit/min
advantages disadvantages
Related to canula placement
 Improved HD stability

 Pro inflamatory mediators

 Improved perfusion of organs

Major neurovascular injury

 Splanchnic decompression

Haematoma
 ↓ RBC and fluid requirements

 ↓ renal and metabolic impairment  Time and cost

 ↓ pulmonary edema Air embolism

Anesthesia for Liver
Transplantation
Preinduction
Induction, preparation for surgery, and maintenance
Preanhepatic phase
Anhepatic phase
Venous reperfusion of the graft
Neohepatic phase
Emergence/transport to ICU
Preinduction

A panorama-Multiple user interfaces, cables, monitoring lines,

and infusions must be well organized.
at least two anesthesiology personnel
final evaluation of the patient
Last-minute laboratory results
consult with the blood bank.
Initial peripheral IV access. Large bore 14g for volume resuscit
ECG
SPO2
IBP
CVP
PA after induction
NMT
BIS

 TEE-- management of fluid therapy

-monitoring of cardiac function

- identification of intraoperative complications(e.g., PE)

Anesthetic Induction and Maintenance
rapid sequence induction is the norm, with cricoid
pressure
denitrogenation is important
Induction-thiopentone,propofol,etomidate
muscle paralysis is obtained with succinylcholine
All volatile agents except halothane are suitable.
Isoflurane and desflurane are used routinely
Nitrous oxide avoided for gastric distension
Opioids –fentanyl,sufentanyl,remifentanyl
Muscle relaxants-atracurium.
Avoid drugs causing elevations in ICP
Vasodilatation and encephalopathy make patients with
ESLD sensitive to induction agents. so doses reduced
Antibiotics targeted against skin flora(e.g., cefazolin)
hepatic encephalopathy reduces opioid and anesthetic
requirements. But massive hemorrhage and
resuscitation can diminish the circulating opioid
concentration
Positioning the patient requires special attention.
supporting and padding all of the body.
supine position.with right arm is tucked alongside
Ryles tube for gastric decompression
Patient warming becomes a major issue.
Warming strategies commonly focus on IV fluids and
forced-air warming devices.
warmed-air plenum under the drapes, have become
available.
Warming IV infusions is mandatory
Rapid Infusion Devices.
Common- level 1
Belmont FMS-flow 750ml/min
Haemonetics RIS-1500ml/min
The Preanhepatic Phase
Begins with induction of anaesthesia to clamping of
venacava,portal vein,hepatic artery.
Liver mobilized,vessels clamped and bileduct separated.

problems
1. Hypotension-clamping the portal triad reduces venous
return,sudden decompression of ascitis
Management-
Fluid resuscitation-crystalloids and colloids
may necessitate institution of venovenous bypass
vasopressor administration
2.hemorrhage-surgical cause and coagulopathy from
collaterals
Management-blood,ffp,platelets
Drugs-aprotinin,tranexamic acid,eACA
3.hypocalcemia-infusion of citrate-rich blood products
absent hepatic citrate metabolism
decreased cardiac performance,svr,bp
management-cal gluconate or chloride,
caution-don’t correct aggressively,after reperfusion citrate is
metabolized so hypercalcemia may occur
4.hyponatremia-hypervolemic hyponatremia
Management-avoid overjelous correction-CPM
colloids,dextrose solutions
5.hypokalemia/hyperkalemia-avoid correcting
hypokalemia,blood transfusions,underlying crf.
6.hypothermia-
Management-fluid warmers,warm blankets,air
warmers
7.hypomagnesemia-generally no need for
correction,levels become normal after reperfusion
8. Hypoglycemia-Glucose supplementation- in
Paediatric patients, in fulminant hepatic failure.
9.Renal protection– Diuresis. Loop diuretics,
dopamine, mannitol, fenoldopam.
Considerations in prehepatic phase
CVP<5 mm Hg -higher incidences of postoperative renal
failure so maintain cvp 10-15
changes in cardiac performance-1.hemorrhage 2. dec venous
return
Choice of Vasopressor-
1. Epinephrine and norepinephrine
2. Vasopressin(also effective for HPS)
 Transfusion and Other Therapies-consider red cell
mass,intravascular volume,plasma oncotic
pressure,electrolytes,glucose clotting factors and platelets
 Colloid for intravascular volume loss
 Plasma oncotic pressure-colloid,FFP,albumin
Albumin-in normal coaggulation status
FFP- hypocoaggulable stautus
Maintain slightly hypocoaggulable state-avoid hepatic or
portal venous thromboses.
Coagulation is monitored-
1.Basic tests-PT,APTT,D-DIMER,FIBRINOGEN
2. Thromboelastography- information about clot lysis
Predictable course of coagulation-
 start hypocoagulable→FFP intraop →maintain
coaggulation→ reperfusion -clot lysis syndrome or DIC
Volume replacement therapy should aim to preserve or move
clotting potential toward a normal state
Antifibrinolytics procoagulants used prophylactically
 Anhepatic Phase
Time from explantation of the diseased liver to reperfusion
of the new liver.
Problems-
Significant acidosis after clamping of vessels
drugs dependent on hepatic metabolism-accumulate after
vessels clamped.doses should be titrated
Immunosuppressant drug medication
Steroid administration (e.g., 100 mg methylprednisolone)
Hemodynamics frequently stabilize during the anhepatic
phase-piggy back technique,
Hypotension→excess fluids →hypervolemia-use inotropes
Lower extremity and splanchnic congestion
arterial blood gases, serum electrolytes, red cell mass, and
laboratory measures of clotting is mandatory
Electrolyte Management- wide rapid swings
Metabolic acidosis-portal and caval cross clamping,low
ph blood transfusions
 ability to clear organic acids is lost
 Hyperventilation or Sodium bicarbonate can be
administered to correct acidemia
 new liver clears citrate and organic acids-rebound
alkalosis
Hypocalcemia- depresses inotropy,vascular tone,clotting
factor deactivation.
goal of intraoperative calcium management is achieving
the lowest ionized calcium concentration consistent with
good cardiac performance and coagulation, typically 0.9–
1.0 mmol/L
Hyponatremia
Glucose management- hepatectomy causes intraoperative
hypoglycemia.
Renal Protection-renal failure- 5–10%
1. maintaining adequate circulating volume
2. splanchnic vasodilators like Dopa and Fenoldopa
3.Intraoperative renal replacement therapy
Neohepatic Phase
begins with the initial reperfusion of the liver
acute clot lysis syndrome frequently- bleeding from
previously coagulated sites in the surgical field.
Elevation of the PT,APTT
Net increase in t-PA,hyperfibrinolysis.decreased
plasminogen activity and increased fibrinogen
products.
TEG-poor clot initiation and rapid dissolution
use of antifibrinolytic agents such as aprotinin,
tranexamic acid, and EACA
may increase the incidence of thrombotic events
Control fibrinolytic event-procoagulant agents
Biliary drainage reconstruction-straight or
choledochojejunostomy with t tube
Post reperfusion syndrome can occur
Massive transfusion complications-
acidosis,coagulopathy and hypothermia
Graft working status-colour texture,bile
production,resolving hypocalcemia,acidosis
Reperfusion of the Graft
After completion of anastamosis caval and portal clamps
opened
 Severe hemodynamic instability
 Persistent hypotension
 Geater than 30% of the anhepatic MAP within 5 minutes
sustained for at least 1 minute
 Asystole
 Significant arrhythmias
 Development of significant fibrinolysis
 Increased PAH,RV pressures-paradoxixal embolism
 Risk factors-
 volume status of the recipient
 myocardial depression due to embolization of cold
preservative solution,hyperkalemic solution
 release of vasoactive pro-Inflammatory factors
 Air and thromboembolism
intraoperative management of PRS
 Optimization of volume status
 vasodilating agents such as prostaglandin or calcium
channel blockers
 Flushing
 100% O2, ACLS
 Inotropic support
 Aggressive correction of electrolyte & acid base imbalance
Increeased PAH→ central venous congestion → reduce
the hepatic perfusion pressure → liver becomes
engorged
Mimics acute rejection of graft
keep the CVP low at the time of reperfusion
PAH patients-Pulmonary vasodilators
lungs are hyperventilated to raise the pH
Nitric oxide
Shifted to ICU
Prepare for early postop care and extubation
Safe operating room extubation after liver
transplantation score
Major criteria ≥7 packed red blood cells intraoperatively
End of surgery lactate ≥3.4 m mol/L
Minor criteria Patient not at home at the time before
surgery
Duration of surgery ≥5 h
Vasoactive drug infusions
Consider extubation if patient has less than two major, less
than three minor
or one major and two minor
Predictors of outcome of liver transplant

 Haemodynamic stability.

 Transfusion requirement.
 Intraoperative bile production.
 Intraoperative urine output.
 Improvement in acidosis.
 Rise in core temperature.
Thromboelastography [TEG]
Global information on the dynamics of clot development,
stabilisation and dissolution that reflect in vivo haemostasis
Methodology developed by Hartet in 1948, Heidelberg,
Germany
Has not been used in clinical practice for more than 25
years
A whole blood sample (citrated or non-citrated) is placed
into a cuvette and a cylindrical pin is immersed.
The pin is free-pending and the cup oscillates.
The clotting process is detected via a torsion wire.
Whole or citrate blood
Coagulation indices-
1.CI-coagulation index
2.Sheer Elastic Modulus Strength – G value
Fibrinolysis
1.Clot lysis index CLI
Platelet mapping assays
Somewhat insensitive to the platelet effects of aspirin
Rotational Thromboelastometry
Sample Type –Citrate (May be used immediately)
Coagulation Index (CI)
Sheer Elastic Modulus Strength– G- value (MCE)
Maximum Lysis (ML)
Platelet mapping not offered on ROTEM
Post transplant complications
INFECTIOUS COMPLICATIONS
Most common-first 6 months-intense
immunosupression
Initial one month surgery related infections-
staph,entterococci,activation of HSV
2-6 months-opportunistic –
CMV,fungal,P.Carinii
>6 months- Influenza,parainfluenza,RSV
 AKI
10% progressing to endstage renal failure
Hypotension-vasodilatation at induction,
hemorrhage,IVC clamping, and reperfusion, Cirrhotic
cardiomyopathy, pretransplant beta-blockade, and
autonomic polyneuropathy
Renal protection-V-V bypass,piggy back technique, N-
acetyl cysteine, nitric oxide, prostanoids, dopamine,
and diuretics
postoperative AKI-bacterial
infections,retransplantation,increased intra abdominal
pressure,calcineurin inhibitors
Institute RRT
 WEANING FROM MECHANICAL
VENTILATION
Risk Factors for Delayed Extubation in LT Patients:
Severity of liver disease before surgery (Child-Pugh)
Age
Duration of graft ischemia
Duration of surgery
Primary graft dysfunction
Intraoperative blood requirements
Body temperature on ICU admission
Renal dysfunction
Hepatic encephalopathy
Need for inotropes or vasopressors
Inadequate oxygenation
Aim for early extubation
 POORLY FUNCTIONING ORGAN
GRAFTS
Hepatic Artery Thrombosis (HAT):3% of cases, is the
most common technical complication
Fulminant hepatic ischemic necrosis, progressive
sepsis, fever, AMS, hypotension, and coagulopathy
duplex Doppler ultrasound for diagnosis, celiac
angiography, computed tomography and magnetic
resonance angiography
Catheter directed thrombolysis, operative arterial
reconstruction, retransplantation
Portal Vein Thrombosis (PVT):0.5% to 15%,
transaminitis, ascites, intestinal congestion, systemic
inflammatory responses due to bacterial translocation,
and gastrointestinal bleeding.
immediate operative thrombectomy may allow graft
salvage, emergent retransplantation.
Hepatic Vein Thrombosis (HVT):
Common with piggy back technique
Nontechnical Complications
Donor/Procurement-Related Factors
Steatosis.
Ischemia/Reperfusion (I/R) Injury
Warm Ischemia Time
Small-for-Size Syndrome (SFSS)-liver volume
required to avoid SFSS is characterized by a graft-to-
recipient weight ratio of 0.8
Large-for-Size Syndrome (LFSS). pediatric recipients,
grafts with body surface area ratios > 1.4
Requirement for RRT
Early Immunological Complications
Retransplantation