• Users Online: 5478
  • Print this page
  • Email this page

Year : 2007  |  Volume : 51  |  Issue : 6  |  Page : 464-471 Table of Contents     

Anaesthesia for liver transplantation: an update

MD, PDCC Neuroanaesthesiologist & Intensivist, Dept of Anaesthesiology, Army Hospital, (R&R), Delhi, India

Date of Acceptance15-Sep-2007
Date of Web Publication20-Mar-2010

Correspondence Address:
TVSP Murthy
Sr Adv ( Anaesth & Neuro), Dept of Anaesthesia, AHRR, Delhi Cantt - 110010
Login to access the Email id

Source of Support: None, Conflict of Interest: None

Rights and PermissionsRights and Permissions

A significant progress has been made in the last two decades in the field of orthotopic liver transplantation since it was first performed in 1967. It now stands as a standard therapy for many patients with acute and chronic liver disease. The success in this field is due to the advancements and innovations which evolved - in the form of better pre and post transplant care, improved anaesthesia, innovative surgical strategies, early detection of complications and progress in the field of immunosuppression. Liver transplantation is now a routine procedure in numerous medical centers throughout the world. The issues involved in the conduct of anaesthesia in this novel procedure are highlighted.

Keywords: Liver transplantation; Anaesthesia, Monitoring

How to cite this article:
Murthy T. Anaesthesia for liver transplantation: an update. Indian J Anaesth 2007;51:464-71

How to cite this URL:
Murthy T. Anaesthesia for liver transplantation: an update. Indian J Anaesth [serial online] 2007 [cited 2021 Jun 23];51:464-71. Available from: https://www.ijaweb.org/text.asp?2007/51/6/464/61182

   Introduction Top

The role of anaesthesia in orthotopic liver transplantation(OLT) is of paramount importance. The current status of liver transplantation is the product of rapid development in the past two decades. The many advances that have been made in this procedure have not been sequential step by step process, but have been intertwined one with the other to reach the present posi­tion. Advances in pharmacological therapy for coagulopathy and appropriate management of the deli­cate balance between clotting and fibrinolysis during surgery, and prevention of ischaemia - reperfusion in­jury of the graft, in addition to quality care anaesthesia have been the pillars of success.

Liver transplantation was performed initially for primary hepatic malignancy and for end stage chronic liver disease. The improvement in the results was ac­companied by a widening of the spectrum of disease processes deemed amenable to liver replacement and included chronic liver disease from alcohol, viral hepati­tis, fulminant hepatic failure from a variety of causes, inborn metabolic defects without parenchymal disease and hepato cellular carcinomas.

The number of available cadaveric donors is lim­ited, however the number of the patients on the waiting list for orthotopic liver transplantation continues to grow. The new organ allocation policy gives preference to patients who are sicker and are likely to die sooner with­out transplantation. This uses Model for End Stage Liver Disease (MELD) score as a predictor of mortality on the waiting list for liver transplantation [1],[2] .

This score is a continuous, objective disease severity score and prognosticates the risk of death within 3 months and is based on 3 prognostic factors - serum creatinine, serum bilirubin and International Normalized Ratio. This however does not consider the success or results of the transplantation. The idea is to have a less pre transplant mortalityyet predict best survival after transplantation [3] .

   Pre anaesthetic evaluation Top

Pre operative evaluation is performed in two stages. In the early first stage, all orthotopic candidates are ex­amined and evaluated and the later second stage evalu­ation is performed immediately before surgery. This ex­amination is performed when a donor organ has been identified.Assessing any neurologic deterioration since the initial first stage evaluation is necessary and signs of progressive metabolic acidosis, infection or sepsis should be sought. Cardiovascular instability, pulmonary infec­tion, coagulopathy, should be corrected and treated. It should be ensured that patient is in the best condition for surgery. Ideally ascites should be controlled, nutrition improved and prothrombin time returned to normal. Fresh frozen plasma, cryoprecipitate and platelets, besides whole blood be catered for and relevant investigations - Hb, total counts, arterial blood gases, urea, creatinine, liver function test(LFT), liver enzymes and electrolytes including coagulogram be repeated as they serve as a baseline reference.

Preoperative assessment of renal function is criti­cal in the perioperative management of these patients. Poor preoperative renal function is likely to predict poor prognosis and are at a higher risk for intraoperative blood loss, post operative need for dialysis, perioperative mor­bidity and mortality [4]. As serum creatinine is not a sensi­tive index of renal function in these cases creatinine clear­ance will be a more preferred indicator. Hepato renal syndrome should always be suspected as the cause of renal failure and treated aggressively.

   Risk stratification Top

The risk and severity scoring of these patients is based on Child ,Pugh and Turcotte classification , which is based on two clinical and three laboratory variables [Table 1]

Anaesthesia - preparation & premedication: Preoperative counseling often suffices for the patients preparation and allows family interaction with an alert in­dividual before surgery, however to alleviate the anxiety involved some anxiolytic such as benzodiazepine (midazolam) intravenously before transfer to theatre will suffice and ensure a calm patient in the operation theatre.

Induction and intubation: All patients are in­duced in theatre, taking care to use screens if bench work is being performed on the donor liver. The patient is placed on a gel blanket, underneath which is thermo­statically controlled warm water blanket kept at 39 de­grees. A forced air warmer is also used. An ECG moni­tor, pulse oximeter and automatic blood pressure moni­tor are attached to the patient before induction.

Anaesthesia is usually induced with midazolam 1­-2 mg, fentanyl 1-1.5mcg.kg -1 and propofol 1-2 mg.kg -1 . This may be followed by suxamethonium or a non-depo­larizing relaxant. A rapid sequence induction with cri­coid pressure is employed, although in low-risk patients the nasogastric tube is passed before intubation, which avoids a more difficult and potentially traumatic proce­dure later. Anaesthesia is maintained with fentanyl (2-3mcg.kg -1 bolus plus 1-2 mcg.kg -1 .hour -1 , by bolus or in­fusion) or a remifentanil infusion through a dedicated line (5mg diluted in 50ml N/Saline at a rate of 5-30ml.hr­1 ), with air / oxygen / desflurane (E'> 4.0%) or isoflurane. The volatile agent of choice has been isoflurane, which preserves splanchnic blood flow better than other vola­tile agents [5],[6] .Atracurium/cisatracurium infusion is usual [7] , but vecuronium may be preferable in asthmatics.

   Placing of vascular lines - monitoring Top

a. Vascular access

Two large-bore intravenous infusions are set up in the arms. An 8.5F PAC introducer, two 5F catheters and a triple lumen catheter are inserted in the right inter­nal jugular vein. If veno-venous bypass is to be used the 5F catheters are replaced with 10 F.

Great care should be taken if the left internal jugu­lar vein(LIJV) is used for bypass or other large bore cannulae, as this route is associated with a much higher risk of perforation. The patient should be carefully ob­served during infusion of the first few hundred milliliters of fluid. If there is doubt, a test infusion may be indi­cated before starting venovenous bypass.

b. Cardiovascular monitoring: The basic triad of lead CM5, direct arterial pressure and central venous pres­sure are monitored in all patients. Use of a PA catheter is at the discretion of the consultant anaesthetist. If a PA catheter is used and the transplantation is uneventful, it is removed before transfer to ICU / HDU. An obturator should always be placed in any PAC introducer not con­taining a PA catheter before the patient leaves the oper­ating theatre. There is a risk of air embolism later if this is not done.

c. Renal function : A urinary catheter is inserted and the collecting bag positioned at the head of the table where the anaesthetist can see it. The burette should be emp­tied hourly and the urine output recorded at the time of each blood sample.

d. Ventilatory monitoring : Routine inspired/expired gas and vapour monitoring and pulse oximetry are used. A flow-volume loop and airway pressures may also be displayed. Once the desired level of ventilation has been achieved, short-term changes in expired carbon dioxide concentration reflect either changes in pulmonary blood flow (cardiac output) or CO2 released from infused blood or sodium bicarbonate solution. Capnography also pro­vides a means of detecting air embolism. Arterial blood gas measurements are used to corroborate these fig­ures.

e. Temperature monitoring : A temperature probe is inserted into the nasopharynx at the time of induction, which may later be replaced by measurements via the PA catheter.

f. Infection prophylaxis: Antibiotics are first given pre­operatively and repeated at completion of anastomoses if blood loss is greater than about one blood volume. Piperacillin and tazobactum/ fluconazole and gentamycin are the usual antibiotics admisnistered in Kings Hospital, UK. These practices are institutional and based on indi­vidual preferences. All invasive procedures, should be performed using full sterile or at least a no-touch tech­nique.

g.Immunosuppression: During the operation this is lim­ited to methylprednisolone, given intravenously in a dose of 7- 10 mg.kg- 1 at the beginning of the anhepatic phase. Re-transplants, already established on immunosuppres­sion, are usually given their routine medication pre-op­erative and intra-operative bolus steroid is only indicated in exceptional circumstances (e.g. sustained hypoten­sion unresponsive to volume loading). The rest of the im­munosuppression usually starts on day 1 following the procedure, in the intensive care unit.

h.Blood loss salvage and replacement: Each trans­fusion line is connected to a high capacity giving set and blood warmer . The Cell Saver is used when significant blood loss is expected and there are no contraindications. One to two suction lines are supplied with the Cell Saver and citrated saline is added to prevent coagulation in the reservoir. If the patient has a known malignant lesion (typically hepatocellular carcinoma in the setting of hepa­titis B or C cirrhosis), or if the bowel is perforated at any time, autotransfusion should not be used. When the washed cells (suspended in saline with a haematocrit of 55%) are re-infused colloid replacement is also required, usually gelofusine.

i. Coagulation monitoring: a) Preoperative coagula­tion screen and full blood count. b) PT/INR is performed routinely in theatre at least hourly [8] . A full coagulation screen,including plateletcount, fibrinogenlevels andTEG are routinely done, to monitor coagulation [9]. Associated electrolyte abnormalities - hyponatraemia [10] and hypomagnesaemia [11] , require guarded correction.

j. Routine blood product preparation: Routinely at least 10 units of blood are demanded and kept prepared for each adult recipient; a further 10 group- specific units are reserved. 2 units of FFP are supplied and 4 units reserved. An apheresis pack of platelets is to be made available from blood bank on request; further packs need to be ordered basing on requirement for which the blood bank should be geared up to meet the demand. When preoperative FFP and/or platelets have been requested on the patient's assessment form, these products should be available at the time of induction to allow administra­tion before central venous cannulation.

Intraoperatively the coagulation parameters - PT/INR/ TEG checked hourly and if found abnormal, prophylac­tic administration of either FFP 1-2 units.hr -1 and plate­lets (if less than 80,000 ) should be done. High risk pa­tients (those with cirrhosis, portal hypertension, PT > 18 or history of RUQ surgery or bacterial peritonitis) => aprotinin infusion (10,000 units.ml -1 ): 5 ml test dose, and if no anaphylactoid signs after 15 minutes, 2 million units over 30 minutes, followed by 500,000 units per hour to end of surgery. Patients with  Budd-Chiari syndrome More Details or a history of DVT or other thrombotic tendency are ex­cluded. If there is a history of previous administration of aprotinin (especially within 6 months), Tranexamic acid may be preferable given the risk of sensitization to aprotinin. Tranexamic acid dose is 2 grams over 10 min­utes, repeated once if there is clinical evidence of fibrin­olysis.

Significant blood losses ( > 3 times blood volume ) should be managed aggressively with blood, FFP at least 4 - 6 units, cryoprecipitate ( if fibrinogen level < 1.0 ) at least 8 units, 1 or 2 units of platelets if count is less than 80,000. Tranexamic acid 30mg.kg -1 (max 2 gm ) over 10 min­utes. Vasopressin infusion 5 units i.v. over 5 minutes, then 10 -30 units per hour may be tried along with nitro­glycerine ( 0.5 - 5 mcg.kg -1 .min -1 ) if coronary ischemia is a concern.

k. Biochemical monitoring: Samples of arterial blood are taken for analysis of blood gases , electrolytes, lac­tate, Hb%, Mg levels and Glucose monitoring at prede­termined intervals - time of induction, beginning of anhepatic phase, 30-45 minutes later, 30-60secs after reperfusion, when the hepatic artery is unclamped and hourly till closure.

l. Maintenance of renal function and fluid balance: Every effort must be made to maintain urine output dur­ing the procedure, although oliguria is usual and anuria may occur during the anhepatic phase. Crystalloid infu­sion: approx 10 ml.kg -1 4% dextrose in 0.18% saline is given in the first hour of anaesthesia. Thereafter, intra­vascular volume is maintained with gelofusine, with blood products added as indicated by measurements of haematocrit and PT. Mannitol is given as an osmotic diuretic and for a possible reno protective effect. 20% solution may be infused in a dose of 1-1.5 g.kg -1 over 30-60 minutes from the time of trial clamping or just be­fore and during the anhepatic phase. 10% mannitol is used in children, who tend to have a hyperosmolar state and have more robust renal function. Furosemide (20­40 mg in adults), also potentially reno protective, may be given at the beginning of the anhepatic phase, when an abrupt fall or temporary cessation of urine output is usual. If cardiac filling is adequate and systolic BP is < 90, a trial of nor epinephrine (4 mg in 50 ml 5% glucose at 2­-10 ml.hr- 1 ) is warranted. This will often improve urine output. Dopexamine 200mg in 50ml 5% glucose infused at 0.5 - 2ml.hr -1 may be given if blood pressure is ad­equate and urine output fails to respond to volume and the other measures outlined above. The maintenance of urine output is desirable; however, the use of low-dose dopamine for this reason is unproven [12] .

m. Haemodynamics: i. Dissection phase -The ma­jor cardiovascular complications associated with this stage are those related to intravascular volume depletion as a result of blood loss, manipulation of the liver hilum and direct compression of the IVC.

During this period the most important consideration is to maintain intravascular volume by infusion of blood and colloid, depending on the haematocrit and coagula­tion status. Calcium chloride must be added in adequate dose to avoid hypotension (approximately 5 ml per litre of citrated blood products depending on severity of liver dysfunction; less in children).

Toward the end of the dissection phase when the liver has been skeletonised, the surgeon will perform a trial clamping of the infra-hepatic vena cava. This should be maintained for long enough for the anesthetist to judge the cardiovascular effects of the maneuver (30-60 sec­onds). The adequacy of blood replacement and the patient's ability to withstand caval clamping is thereby assessed. If the systolic pressure falls to less than 70% of its previous value, (or SAP < 80-90 mmHg, or MAP < 60mmHg), in the presence of adequate blood replace­ment, or if ECG changes occur, bypass support may be needed.

ii. Venovenous bypass -As long as blood volume is well maintained, hypotension on clamping is infrequent. However, venovenous bypass is often considered for other reasons [13] . These include difficult retrocaval dis­section (needing caval decompression), renal impairment (creatinine > 150, creatinine clearance <50), cardiac ar­rhythmia (atrial fibrillation, persistent nodal rhythm) or impaired systemic perfusion (acidosis, inotrope-depen­dency). A decision to use bypass should always be dis­cussed with the operating surgeon. Abypass technician is available for every adult transplant; who sets up and operates the bypass system, monitoring pressure and flow, and checking for aspiration of air, a potentially fa­tal complication. Flows of 1.5 - 4.5 liters per minute are obtained, depending mainly on the size and position of the femoral cannula and the patient's cardiac output. Great care should be taken if the LIJV is used for by­pass or other large bore canulae, as this route is associ­ated with a much higher risk of perforation. If technical difficulties are encountered during insertion or if free aspiration of blood is not demonstrated, an on-table chest x-ray should be obtained. The patient should be care­fully observed during infusion of the first few hundred milliliters of fluid.

iii. Anhepatic phase - Haemodynamic changes during this period are related to IVC cross-clamping and to physiological changes caused by the removal of the liver. IVC cross-clamping results in a decrease in car­diac output of 40-60%, especially in the absence of ex­tensive collaterals, accompanied by a marked increase in systemic vascular resistance. IVC side-clamping, as­sociated with the cavacavaplasty or "piggyback" tech­nique, obstructs caval flow less, although this is variable. It is unusual to need bypass for haemodynamic stability when this technique is used. Removal of the native liver results in reduction in oxygen consumption, which also contributes to the fall in cardiac output.Absence of liver function results in inability to metabolize citrate; citrate intoxication presents with decreased ionized calciumand myocardial depression. Hypocalcaemia must be cor­rected before reperfusion.

Occlusion of the portal venous outflow will increase portal pressures and may increase surgical bleeding [14],[15] .These can be obviated by using Venovenous by pass, but it has its own inherent side effects of air embolism etc which requires monitoring [16] Piggy back technique decreases the need for VVB [17] . Attempts to increase filling pressures by blood and fluid replacement must be cautious at this stage, because of the danger of fluid overload at the time of liver revascularization, when nor­mal venous return and central blood volume are restored.

iv. Post-anhepatic (reperfusion) phase - Reperfusion of the liver may cause dramatic cardiovas­cular changes [18] . Although these usually last a few min­utes, they may be severe enough to cause cardiac ar­rest. More specifically, typical disturbances are: 1) sig­nificant decreases in heart rate, MAP and SVR. 2) vari­able increases in CVP, PCWP, PVR. 3) cardiac output increases, although a transient decrease due to a fall in heart rate and stroke volume may be observed. It is im­portant to ensure that ionized calcium levels before reperfusion are normal. Treat hypotension with ephe­drine or a low bolus dose of pressor, such as epineph­rine, nor epinephrine, or metaraminol. It is common prac­tice to use one of these prophylactically, along with cal­cium chloride, on unclamping of the portal vein.

Once these acute haemodynamic changes have subsided, the remainder of the operation is typically un­eventful. However, blood loss often continues and may increase in thepresenceof pathological fibrinolysis,which can be managed with either of the antifibrinolytics as per the institutional protocol or individual preference -epsilon aminocaproic acid [19] , tranexamic acid [20] or aprotinin [21] .

n. Specific complications:

i. Metabolic acidosis - Metabolic acidosis de­veloping during the dissection phase of the operation is usually due to tissue hypoperfusion resulting from shunt­ing associated with the liver disease. Treatment should be aimed at correcting the underlying problem, and as­certaining that there is no respiratory component. So­dium bicarbonate should be used guardedly.

After reperfusion of the liver, metabolic acidosis typically worsens as a result of sudden release into the circulation of protons from the ischaemic liver and ob­structed splanchnic bed. This is generally self-limited and resolves over a few hours without specific treatment [22]. Post - reperfusion syndrome is defined as a 30% or more drop in blood pressure from baseline that lasts for 1 minute or more and occurs within 5 minutes of reperfusion [23] . The treatment of post - reperfusion syn­drome includes the maintenance of adequate filling pres­sures, hyperventilation, and administration of calcium chloride and sodium bicarbonate for hyperkalemia and acidosis.

ii. Major bleeding - At times of rapid loss it is essential to transfuse at a rate sufficient to maintain ar­terial and venous pressures in the normal range for an anaesthetised, ventilated patient. It should be remem­bered that concentrated and washed cells must be supple­mented with colloid and that rapid blood replacement will lead to citrate intoxication, hypocalcaemia, and rarely to hyperkalemia.

iii. Hypocalcaemia - Ionised calcium measure­ments are made at regular intervals during the opera­tion. Levels tend to be low even in the early part of the operation in patients with poor liver function, as a result of the citrate in blood products. In spite of calcium ad­ministration, these may fall further during the anhepatic phase, when citrate metabolism presumably ceases. If blood loss is not substantial, values return to normal af­ter reperfusion without the need for further treatment. The aim should be to keep [Ca ++ ] within the normal range (1.1-1.3 mmol.l -1 ) at all times, especially during the pe­riod preceding reperfusion.

iv. Hyperkalemia - This occurs on release of the clamps but the effect is short lasting and no specific treat­ment apart from prophylactic calcium chloride is indi­cated. When hyperkalemia is present or is likely to oc­cur before reperfusion measures to prevent a further marked increase are essential to reduce the risk of hyperkalaemic arrest at reperfusion. These include washing of bank blood, i.v.glucose-insulin (10 units in 50 ml 50% glucose), nebulised salbutamol (10mg), i.v. furo­semide and sodium bicarbonate (50-100 mmol).

v. Changes in blood glucose - The blood glucose level tends to rise throughout the operation, largely due to the glucose given with bank blood. Hypoglycaemia may nevertheless occur toward the end, due presum­ably to uptake by the new liver. It has not been our rou­tine practice to give insulin to correct hyperglycaemia, although infusion of 2-5 units per hour may be advisable if the concentration exceeds 12 -15 mmol.l -1 .

vi. Arrhythmias - Supraventricular and ventricu­lar arrhythmias during the dissection and anhepatic phases may be treated initially with magnesium, unless preoperative Mg ++ values are raised (they are typically normal or mildly depressed and ionised values fall with blood transfusion (citrate effect). Magnesium bolus dos­age at the rate of 8mmol (4ml 50% MgSO4 ) over 20 minutes; may be diluted in N/Saline and given by syringe pump. Potassium may be indicated if <3.0 mmol.liter -1 , but should be carefully titrated.Acute digitalisation may rarely be indicated for new-onset atrial fibrillation; amiodarone is effective in this context but may be haz­ardous, especially during the anhepatic phase, since it impairs compensatory vasoconstriction.

Sinus slowing always occurs on reperfusion, pos­sibly caused by the transient but marked hyperkalaemia, or by the effect of the rapid temperature change on the sino-atrial node as the cold hepatic effluent enters the circulation. However, overt bradycardia is unusual in the absence of severe hyperkalaemia.Atrial irritability is not uncommon at reperfusion, although it is typically tran­sient and treatment is rarely required.

vii. Initial poor graft function - This is associ­ated with the following signs after reperfusion: sustained metabolic acidosis, a greyish macroscopic appearance of the liver, a persistently raised PT accompanied by clinicalcoagulopathy(fibrinolysis), persistentoliguria,sus­tained vasodilation and hypotension. Management in­cludes: N-acetylcysteine 10g (= 50ml) @ 4ml.hr -1 (= 800mg/hr), Dopexamine 1- 4 (max 6) mcg.kg -1 .min -1 (200mgin 50ml5% dextrose), Norepinephrine(4mg/50ml 5% dextrose) @ 2-20ml.hr -1 or Dopamine at vasoconstricting dose (200mg in 50ml 5% destrose) @ 5-20ml.hr -1 if hypotension persists after adequate filling. Care should be taken to avoid overfilling since raised hepatic venous pressure may impair liver perfusion. "Marginal" livers are at a higher risk for primary non­function and delayed graft function [24] . The accepted cri­teria for marginality include - age >60 years, number of hospital days>5 days, systolic hypotension< 70 mm Hg >1 hour, use of 2 or more vasopressors, cardiac arrest duration >30 min, peakserumsodium >165 mEq.L -1 , liver enzymes >3 times normal, microvesicular fat content >25%, non-heartbeating donors, and prolonged cold is­chaemia time.These are more prone for ischaemia reperfusion injury compared to normal grafts. Manage­ment of these patients during reperfusion is critical. There is a greater release of K + from the donor liver during reperfusion, resulting in hyperkalemia. Increase in the incidence of hypotension, increase in pulmonary-artery pressures, right ventricular dysfunction and failure, and dysrhythmias leading to cardiac arrest have all been ob­served. This could be avoided to a large extent by proper flushing of the liver before grafting [25] and by initial arte­rial anastomosis and arterial flushing..

viii. Cardiac arrest - The usual cause is acute hyperkalaemia at reperfusion. VF, asystole and pulseless electrical activity (PEA) are all treated initially with epi­nephrine. If cardiac arrest is considered likely the defibril­lator should be immediately available and sterile wrapped internal paddles given to the circulating nurse. Cardiac compression is performed by the surgeon using a bi­manual technique, stabilising the diaphragmatic surface of the heart with the palm of one hand whilst compress­ing the sternum with the heel of the other. Full internal cardiac massage is difficult to perform safely via an ab­dominal incision; rupture of the right ventricle may eas­ily occur. DC cardioversion is carried out using external electrodes (200, 200, 360J), depending on ease of ac­cess.

If VF/pulseless VT associated with hyperkalaemia is persistent after full with epinephrine, sodium bicar­bonate and glucose / insulin, consideration can be given to the following: 1.Reclamping the portal vein,2.Magnesium (especially if Mg++ low preopera­tively) 4 mmol over 10 minutes and repeated if needed,3.Amiodarone 100-200 mg slow iv bolus.

Post operative care after OLT: A recent trend has been to fast-track patients after OLT. Routine post­operative ventilation of all patients after OLT is unnec­essary. Carefully selected patients can be extubated in the immediate post operative period in the intensive care unit. Avoiding positive pressure ventilation in the perioperative period may be beneficial in limiting the decrease in blood flow to the newly grafted liver. How­ever, this requires experienced personnel to manage post­operative pain. To successfully fast track, the following are important: modifying anaesthetic technique by utiliz­ing short-acting drugs, use of neuromuscular blockers such as cisatracurium, which is independent of organ function, minimizing use of narcotics and benzodiazepine, and appropriate titration to permit spontaneous breath­ing and awakening at the end of surgery.

Patients who are obese or who have a poor Child's Pugh Score, poorly controlled ascites, encephalopathy, large intraoperative blood loss, and multiple organ trans­plantation are probably not appropriate candidates. Fur­thermore, obesity (BMI >32) and preoperative encepha­lopathy are likely to result in failed attempts at immedi­ate extubation. Endotracheal extubation of a patient at the end of surgery and discharge to the intensive care unit is unlikely to result in a shorter intensive-care-unit stay or in significant cost savings because of the quirks of intensive-care-unit discharge criteria [26] . Furthermore, even if the patient is extubated, close haemodynamic and other monitoring may be essential.

   Conclusion Top

Excellent progress has been made in the under­standing of various complex physiological issues that are integral to the successful management of patients un­dergoing OLT. As a result, many of the changes that occur during OLT are predictable and safely managed [27],[28] . Advances in pharmacological therapy for coagulopathy and appropriate management of the deli­cate balance between clotting and fibrinolysis will en­hance future management. Further research is needed in the prevention of postreperfusion haemodynamic changes that occur because of ischaemia-reperfusion injury of the graft.

   References Top

1.Kamath PS, Wiesner RH, Malinchoc M, et al. A model to predict survival in patients with end-stage liver disease. Hepatology 2001;33:464-470.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.United Network for Organ Sharing Liver Disease SeverityScore CommitteeWiesner R, Edwards E, et al. Model for endstage liver disease (MELD) and allocation of donor livers. Gastroen­terology 2003;124:91-96.  Back to cited text no. 2      
3.Giannini E, Botta F, Testa R. Utility of the MELD score for assessing 3-month survival in patients with liver cirrhosis: one more positive answer. Gastroenterology 2000; 125:993-994.  Back to cited text no. 3      
4.Pham PT, Pham PC, Wilkinson AH. The kidney in liver trans­plantation. Clin Liver Dis 2000;3:567-590.  Back to cited text no. 4      
5.O'Riordan J, O'Beirne HA, Young Y, Bellamy MC. Effects of desflurane and isoflurane on splanchnic microcirculation dur­ing major surgery. Br J Anaesth 1997; 78:95 - 6.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]  
6.Gatecel C, Losser MR, Payen D. The postoperative effects of halothane versus isoflurane on hepatic artery and portal vein blood flow in humans. Anesth Analg 2003; 96:740- 5.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.De Wolf AM, Freeman JA, Scott VL, Tullock W, Smith DA, Kisor DF, et al. Pharmacokinetics and pharmacodynamics of cisatracurium in patients with end-stage liver disease undergo­ing liver transplantation. Br J Anaesth 1996; 76:624- 8.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Kang Y. Transfusion based on clinical coagulation monitoring does reduce hemorrhage during liver transplantation. Liver Transpl Surg 1997; 3:655- 9.  Back to cited text no. 8  [PUBMED]    
9.Ozier Y, Pessione F, Samain E, Courtois F. Institutional vari­ability in transfusion practice for liver transplantation. Anesth Analg 2003; 97:671-9.  Back to cited text no. 9      
10.Wszolek ZK, McComb RD, Pfeiffer RF, Steg RE, Wood RP, Shaw BW, et al. Pontine and extrapontine myelinolysis follow­ing liver transplantation. Relationship to serum sodium. Trans­plantation 1989;48:1006- 12.  Back to cited text no. 10      
11.Scott VL, De Wolf AM, Kang Y, Altura BT, Virji MA, Cook DR, et al. Ionized hypomagnesemia in patients undergoing orthotopic liver transplantation: a complication of citrate in­toxication. Liver Transpl Surg 1996; 2:343- 7.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]  
12.Swygert T. Effect of intraoperative low-dose dopamine on re­nal function in liver transplant recipients. Anesthesiology 1991;75:571-6.  Back to cited text no. 12      
13.Bogdonoff DL, Spiekermann BF: Should acidosis during liver transplantation be treated?Anesthesiology1997; 82:1540-1541.  Back to cited text no. 13      
14.Haagsma EB, Gips CH, Wesenhagen H, Van Imhoff GW, Krom RA. Liver disease and its effect on haemostasis during liver transplantation. Liver 1985;5:123 - 8.  Back to cited text no. 14  [PUBMED]    
15.Bechstein WO, Neuhaus P. Bleeding problems in liver surgery and liver transplantation. Chirurg 2000;71:363- 8.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]  
16.Budd JM, Isaac JL, Bennett J, et al. Morbidity and mortality associated with large-bore percutaneous venovenous bypass cannulation for 312 orthotopic liver transplantations.Liver Transplant 2001: 7:359-362.  Back to cited text no. 16      
17.Tzakis A, Todo S, Starzl TE. Orthotopic liver transplantation with preservation of the inferior vena cava. Ann Surg 1989; 210:649- 52.  Back to cited text no. 17  [PUBMED]  [FULLTEXT]  
18.Blanot S, Gillon MC, Ecoffey C. Circulating endotoxins during ortholopic liver transplantation and post-reperfusion syndrome [letter]. Lancet 1993:342:859-60.  Back to cited text no. 18      
19.Kang Y, Lewis JH, Navalgund A, et al. Epsilon-aminocaproic acid for treatment of fibrinolysis during liver transplantation. Anesthesiology 1987; 66:766-73.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]  
20.Dalmau A, Sabate A, Acosta F, et al. Tranexamic acid reduces red cell transfusion better than epsilon-aminocaproic acid or placebo in liver transplantation. Anesth Analg 2000;1:29-34.  Back to cited text no. 20      
21.Porte RJ, Molenaar IQ, Begliomini B, et al. Aprotinin and transfusion requirements in orthotopic liver transplantation: a multicenter randomized double-blind study. Lancet 2000;355:1303- 1309.  Back to cited text no. 21  [PUBMED]  [FULLTEXT]  
22.Aggarwal S, Kang Y. Freeman JA. Fortunato FL. Pinsky MR. Postreperfusion syndrome: cardiovascular collapse following hepatic reperfusion dluring liver transplantation. Transplant Proc 1987;19:54S-55S.  Back to cited text no. 22      
23.Estrin JA, Beiani KG, Ascher ML, Lura D, Payne W, Najarian JS. Hemodynamic changes ondumping and unclamping of ma­jor vessels during liver transplantation. Transplant Proc 1989:21:3500-5.  Back to cited text no. 23      
24.Busuttil RW, Tanaka K. The utility of marginal donors in liver transplantation. Liver Transplant 2003;9:651-663.  Back to cited text no. 24      
25.Krasko A. Liver failure, transplantation, and critical care. Crit Care Clin 2003;19:155-83.  Back to cited text no. 25      
26.Findlay JY, Jankowski CJ, Vasdev GM, et al. Fast track anes­thesia for liver transplantation reduces postoperative ventila­tion time but not intensive care unit stay. Liver Transplant 2002; 8:670-675.  Back to cited text no. 26      
27.Karam V, Castaing D, Danet C, et al. Longitudinal prospective evaluation of quality of life in adult patients before and one year after liver transplantation. Liver Transplant 2003;9:703­-711.  Back to cited text no. 27      
28.Gundappa Neelakanta, Seminars in Anesthesia, Perioperative Medicine and Pain 2004;23;1:52-61.  Back to cited text no. 28      


  [Table 1]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
    Pre anaesthetic ...
    Risk stratification
    Placing of vascu...
    Article Tables

 Article Access Statistics
    PDF Downloaded1950    
    Comments [Add]    

Recommend this journal