INTRODUCTION — This topic will discuss anesthetic management during liver transplantation, including postoperative pain management.
The preanesthetic consultation and preparations for liver transplantation are discussed in a separate topic. (See "Liver transplantation: Preanesthetic consultation and preparations".)
Intravascular access — Reliable large bore venous access is necessary for administration of intravenous (IV) fluids, blood products, and vasopressors. Rapid transfusion devices are nearly always employed since massive blood loss is possible during various phases of liver transplantation surgery (see 'Specific considerations for each surgical phase' below). We typically insert a central venous catheter (CVC) into an internal jugular vein after induction of general anesthesia but before surgical incision. We use ultrasound guidance, which reduces risk of hematoma in patients with coagulopathy, and detects thrombi in the internal jugular vein in those with hypercoagulability. (See "Liver transplantation: Preanesthetic consultation and preparations", section on 'Disorders of coagulation' and "Basic principles of ultrasound-guided venous access".)
In many centers, a second peripheral large-bore rapid infusion catheter is also inserted [1,2].
Monitoring considerations — Intraoperative monitoring practice patterns in liver transplant centers have been assessed by the Liver Transplant Anesthesia Consortium, and are reflected in the recommendations below [1,2].
•Intra-arterial monitoring – We typically place a radial arterial catheter in the right or left wrist (depending on planned intraoperative positioning of the patient) before induction of anesthesia, although many centers place this catheter shortly after induction (see 'Induction of general anesthesia' below). A second arterial catheter is placed in the femoral artery or the opposite radial artery as back-up in most centers, in case the first catheter fails [1,2]. Generally, a femoral artery is preferred for the second site because femoral arterial blood pressure (BP) measurements are typically more reliable than those from the smaller radial arterial site, particularly during infusion of high vasopressor doses. In some instances, retraction of the rib cage to obtain adequate surgical visualization can compress the subclavian artery against the first rib; in such cases the femoral arterial pressure can be 10 to 20 mmHg higher than the radial arterial pressure for the duration of the retraction . (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation".)
•Central venous catheter – As noted above, a CVC is typically inserted into an internal jugular vein (see 'Intravascular access' above), and one port is used to monitor central venous pressure (CVP). Although not a reliable indicator of intravascular volume status, continuous measurement of CVP allows recognition of directional changes. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)
•Pulmonary artery catheter – A pulmonary artery catheter is still routinely used in most centers for liver transplant patients to monitor cardiac output (CO), pulmonary artery pressure, and increases in pulmonary vascular resistance (PVR) [1,2]. We employ a pulmonary artery catheter with capabilities to measure continuous CO and mixed venous oxygen saturation (SVO2).
Patients in liver failure have a baseline vasodilatory state compensated by elevated CO to preserve perfusion of vital organs (see "Liver transplantation: Preanesthetic consultation and preparations", section on 'Cardiopulmonary changes'). Thus, it is important to detect any decrease in CO since this may portend cardiovascular collapse (eg, sudden deterioration of right ventricular [RV] function due to sudden increases in PVR). Notably, continuous CO values may not be reliable during large volume resuscitation; however, SVO2 measurements generally remain accurate. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".)
•Transesophageal echocardiography – Transesophageal echocardiography (TEE) is often used to monitor hemodynamics and to diagnose causes of hemodynamic instability (eg, exacerbation of preexisting conditions or new adverse events) [4-21]. Specific examples that may cause sudden severe hypotension include [7-9,16,20,22-33]:
-Hypovolemia due to sudden reductions in preload due to bleeding or inferior vena cava (IVC) manipulation
-Low systemic vascular resistance (SVR) refractory to vasopressors due to liver failure, cirrhotic cardiomyopathy or post-reperfusion syndrome (see 'Post-reperfusion syndrome' below)
-Myocardial systolic dysfunction due to cirrhotic cardiomyopathy (with relative volume overload)
-Diastolic dysfunction due to cirrhotic cardiomyopathy
-RV distention and failure caused by acute changes in filling pressures due to rapidly occurring volume shifts or changes in PVR after release of toxic metabolites or pulmonary emboli
-Severe myocardial ischemia
-Thromboembolic phenomena including air emboli or formation of thrombi in the LV, RV, or IVC, due to a pre-existing prothrombotic state in end-stage liver disease, as well as air or thrombotic pulmonary emboli (see "Liver transplantation: Preanesthetic consultation and preparations", section on 'Disorders of coagulation')
-Presence of stenosis of the hepatic vein or IVC
A nasogastric tube is typically inserted gently before TEE probe insertion to empty the stomach, and also improve visibility within the surgical field by reducing gastric distention. Many liver transplant recipients have esophageal varices and higher risk (see "Liver transplantation: Preanesthetic consultation and preparations", section on 'Esophageal pathology'). We employ extra lubrication for the nasogastric tube and the TEE probe, with careful gentle insertion to minimize this risk. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Contraindications and precautions'.)
•Other cardiovascular monitors – Other devices to assess CO and intravascular volume status are used in some liver transplant centers [34-37]. (See "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Cardiac output' and "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Volume tolerance and fluid responsiveness'.)
•Intracranial pressure monitoring – In selected patients with severe encephalopathy and elevated intracranial pressure, invasive intracranial pressure monitoring may have been established in the preoperative period to optimize cerebral perfusion. If present, this monitoring is continued throughout the transplantation including the neohepatic phase . (See "Liver transplantation: Preanesthetic consultation and preparations", section on 'Acute liver failure with increased intracranial pressure'.)
•Cerebral oximetry – Although neuromonitoring with cerebral oximetry using near-infrared spectroscopy is not common, some centers use this technology to recognize impaired cerebral autoregulation and track cerebral deoxygenation during the anhepatic phase, as well as hyperoxygenation during the reperfusion phase [38,39]. (See 'Anhepatic phase' below and 'Reperfusion phase' below.)
Antibiotic prophylaxis — Prophylactic antibiotics should be administered before the surgical incision. Selection is based on the center's routine protocols for abdominal/biliary surgery. (See "Antimicrobial prophylaxis for prevention of surgical site infection following gastrointestinal procedures in adults".)
Induction of general anesthesia — We induce general anesthesia after placement of an intra-arterial catheter to continuously monitor BP. For patients with inadequate time for fasting and those with increased intra-abdominal pressure due to moderate or severe ascites, rapid sequence anesthetic induction and endotracheal intubation is typically employed with appropriate additional precautions against aspiration. Succinylcholine can be used as a rapid-acting neuromuscular blocking agent (NMBA) during rapid sequence induction and intubation in patients without hyperkalemia. Although a non-depolarizing NMBA that is not metabolized by the liver (eg, cisatracurium) is an alternative, slower onset of action is not optimal for rapid sequence induction and intubation. (See "Rapid sequence induction and intubation (RSII) for anesthesia".)
Many clinicians select propofol for anesthetic induction in patients without severe comorbidities. However, propofol doses are typically decreased, and coadministration of vasopressor drugs is often necessary to maintain hemodynamic stability. In patients with end-stage liver disease, BP and CO are maintained by activation of the sympathetic system to compensate for chronically low SVR (see "Liver transplantation: Preanesthetic consultation and preparations", section on 'Cardiopulmonary changes'). Since this sympathetic drive is decreased by induction of general anesthesia, severe hypotension may occur. Alternatively, induction with etomidate or ketamine or a narcotic-based induction may be used for patients when hemodynamic instability is of particular concern. (See "General anesthesia: Intravenous induction agents" and "Perioperative uses of intravenous opioids in adults: General considerations", section on 'High-dose opioid induction technique'.)
MANAGEMENT DURING THE TRANSPLANTATION PROCEDURE
Maintenance of general anesthesia — Either inhalation or intravenous (IV) agents may be employed to maintain general anesthesia during liver transplantation.
Compared with patients with normal liver function, patients with end-stage liver disease require a lower minimum alveolar concentration (MAC) of a potent inhalation anesthetic to prevent motor responses to initial skin incision (eg, for sevoflurane, approximately 1.3 percent compared with 1.7 percent) .
Total intravenous anesthesia (TIVA) has also been used for maintenance of general anesthesia during liver transplantation, particularly if the aim is to achieve tracheal extubation in the operating room immediately after transplantation . Propofol is typically selected as the primary agent for maintenance of a TIVA technique. Despite a larger volume of distribution, propofol dosing need not be significantly adjusted for patients with liver disease; however, recovery from propofol is typically delayed due to greater sensitivity to its pharmacodynamic effects  (see "Anesthesia for the patient with liver disease", section on 'Sedative hypnotics'). Although a continuous infusion of cisatracurium is often selected (see "Anesthesia for the patient with liver disease", section on 'Neuromuscular blocking agents'), higher doses are typically required and recovery may be prolonged, possibly due to increased extracellular fluid and increased volume of distribution in patients with end-stage liver disease compared with those with normal liver function .
Hemodynamic and vasopressor management — We maintain a mean arterial pressure (MAP) ≥65 to 75 mmHg throughout all phases of liver transplant procedures. A higher target may be selected for patients with preexisting hypertension. Most patients require vasopressor therapy in various phases of the transplant procedure to maintain adequate MAP due to the chronic vasodilatory state associated with end-stage liver disease, the superimposed vasodilatory effects of general anesthetic agents, as well as preload and afterload changes and severe metabolic abnormalities during various phases of the surgical procedure. (See 'Specific considerations for each surgical phase' below and "Liver transplantation: Preanesthetic consultation and preparations", section on 'Cardiopulmonary changes'.)
There is no general consensus regarding choice of vasopressors (table 1) . We routinely administer norepinephrine 2 to 10 mcg/minute (0.03 to 0.15 mcg/kg per minute), and add vasopressin 0.01 to 0.04 units/minute to compensate for endogenous vasopressin deficiency if the patient is hypotensive and vasodilated during any stage of the liver transplant. Vasopressin also beneficially reduces portal hypertension by decreasing portal venous flow and pressure and increasing hepatic arterial flow [45,46].
Dobutamine, dopamine, and/or epinephrine may be added to provide inotropic support when appropriate. For example, we occasionally add an epinephrine infusion during the anhepatic phase and/or after reperfusion if blood pressure (BP) remains marginal despite high dose of both norepinephrine (eg, >15 mcg/minute) and vasopressin (eg, >0.1 units/min).
Blood and coagulation management — Transfusions of red blood cells (RBCs) and other blood products (eg, fresh frozen plasma [FFP] or prothrombin complex concentrate [PCC]; cryoprecipitate or fibrinogen concentrate; or platelets) are usually necessary during liver transplantation. Information rapidly derived from intraoperative laboratory testing for anemia and for coagulopathy allows rational decision-making regarding transfusion of RBCs and other blood components. (See "Intraoperative transfusion and administration of clotting factors", section on 'Intraoperative diagnostic testing'.)
Management of anemia
●Blood salvage – To avoid or minimize allogeneic blood transfusion, most liver transplantation centers employ intraoperative blood salvage using a cell saver system to separate, wash, and concentrate salvaged red blood cells (RBCs) for reinfusion in most patients [1,2]. Contraindications include presence of cancer (hepatocellular carcinoma), localized infection, or otherwise contaminated surgical field. Suctioning of ascites, bile, and intestinal content into the cell saver system is avoided. (See "Surgical blood conservation: Blood salvage".)
Notably, there are no coagulation factors in cell saver blood because plasma is washed away and replaced with 0.9% saline; thus, dilutional coagulopathy may occur. Since salvaged blood does not contain any significant amount of potassium after the washing process, it can be transfused even if severe hyperkalemia is present, and is preferred rather than transfusion of allogeneic RBCs from the blood bank. Another option is washing of fresh blood with the cell saver before transfusion into a hyperkalemic patient.
●Red blood cell transfusion – Transfusion of RBCs and other blood products is usually necessary during liver transplantation surgery, although surgery without transfusion has become more common with use of strategies such as intraoperative blood salvage and antifibrinolytic administration . (See "Perioperative blood management: Strategies to minimize transfusions".)
A sufficient reserve of blood products should be immediately available in or near the operating room. Use of a rapid transfusion system is often necessary. (See "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells' and 'Pre-anhepatic (dissection) phase' below.)
Decisions to transfuse salvaged or allogeneic blood are guided by balancing risks of transfusion with risks of anemia. We use point-of-care (POC) instruments to measure hemoglobin (Hb) for earlier detection of anemia, although these measurements are not as accurate as standard laboratory measurements [48-52]. Typically, the selected Hgb transfusion trigger is <7 to 8 g/dL. However, factors that may necessitate a more liberal transfusion trigger (Hb <9 g/dL) include severity of ongoing and anticipated blood loss and current intravascular volume status. For example, severe bleeding often occurs in the pre-anhepatic phase during surgical dissection of the diseased liver, particularly if the patient has portal hypertension and coagulopathy.
Allogeneic RBCs from the blood bank contain potassium; the concentration increases with age of the RBCs and can be >50 mmol/L . During transfusion of large volume transfusion of RBCs, moderate (>5.5 mEq/L) or severe (>6.5 mEq/L) hyperkalemia may occur. Further transfusion of allogeneic RBC units is stopped until treatment of hyperkalemia has been initiated and lower potassium levels have been confirmed . In some patients, the transplant team may elect to order "prewashing," of some blood bank RBC units to lower their potassium content, or perform intraoperative washing of fresh blood in the cell saver unit. Such washed units are kept in reserve until severe bleeding and hyperkalemia occurs (see 'Hyperkalemia and other metabolic abnormalities' below). Risk for postoperative acute kidney injury may also be increased after transfusion of older RBCs stored for >14 days, possibly due to accumulated proinflammatory substances .
Management of coagulopathy — Coagulation defects in liver disease are complex and may cause profound bleeding diathesis or hypercoagulability with consequent risk of thrombosis [56,57]. (See "Liver transplantation: Preanesthetic consultation and preparations", section on 'Disorders of coagulation'.)
Preoperative coagulopathy is present in many patients with end-stage liver disease. Accelerated fibrinolysis may result in rapid dissolution of clots after formation, thereby contributing to coagulopathy [58-61]. In addition, marginal donor organ quality (for example with a donation after cardiac death donor) may cause a delay in function of the newly grafted liver, which may delay resolution of coagulopathy during the neohepatic phase. (See 'Neohepatic phase' below and 'Persistent bleeding' below.)
Correction of coagulopathy and blood management are further complicated by the complex derangements of the coagulation system that may also lead to hypercoagulability. For example, thrombosis of a tenuous hepatic artery anastomosis may occur more readily if coagulopathy is aggressively corrected, especially if platelets are transfused. (See 'Thromboembolism' below.)
•Standard laboratory tests of coagulation – Standard coagulation tests include prothrombin time, activated partial thromboplastin time, international normalized ratio (INR), and platelet count (see "Clinical use of coagulation tests" and "Platelet function testing"). However, these standard tests may not detect hypercoagulability since they only measure the ability of pro-coagulant cascades to form thrombin (patients with liver disease can have normal or even increased thrombin generation [57,62-64]). However, these standard tests do not assess factors affecting firm clot formation after initial thrombin formation, or factors contributing to clot strength (eg, fibrinogen concentration, platelet function) [57,65].
•Viscoelastic tests – Viscoelastic POC tests of coagulation, such as thromboelastography (TEG) or an adaptation of TEG known as rotational thromboelastometry (ROTEM), are used in many centers to test overall hemostatic function in liver transplantation and other selected procedures (eg, cardiac or trauma surgery) [57,66-70]. A TEG or ROTEM tracing provides information regarding clot initiation (ie, initial thrombin formation), kinetics of ongoing clot formation, eventual clot strength, and clot dissolution via fibrinolysis (figure 1). The table provides guidance for transfusion of specific blood products during liver transplantation surgery based on TEG or ROTEM values (table 2), although decisions also depend on results of standard tests of coagulation, presence of ongoing bleeding, and stage of surgery . Although use of viscoelastic test guidance can reduce transfusions of blood products and specifically FFP during liver transplantation, the effect on outcomes is unclear [57,69-72].
Further information is provided in separate topics. (See "Platelet function testing", section on 'Viscoelastic testing (TEG and ROTEM)' and "Intraoperative transfusion and administration of clotting factors", section on 'Intraoperative diagnostic testing'.)
●Transfusion of blood components
•Fresh frozen plasma or prothrombin complex concentrate – During the dissection phase (see 'Pre-anhepatic (dissection) phase' below), severe preexisting coagulopathy should be corrected [56,57], primarily with the coagulation factors I, II, V, VIII, IX, X, XI, XIII, as well as anticoagulant protein C, protein S, and antithrombin III that are all contained in FFP. Furthermore, FFP is a component of massive transfusion protocols during periods of significant bleeding. However, FFP contains only a small amount of fibrinogen. (See "Intraoperative transfusion and administration of clotting factors", section on 'Plasma' and "Massive blood transfusion", section on 'Approach to volume and blood replacement'.)
FFP should not be transfused based on an elevated INR in the absence of clinical bleeding. Risk of over-transfusion with high volumes of FFP include transfusion-associated acute lung injury (TRALI) and thrombotic complications. Viscoelastic testing can help guide transfusion of FFP (table 2) [57,67,69,70].
A 4-factor PCC may be administered instead of or in addition to FFP, with selection of a product that contains FII, FVII, FIX, FX as procoagulant factors, as well as the anticoagulant factors protein C, protein S, antithrombin III, and a small amount of heparin to decrease risk for excessive thrombin generation (table 3). Advantages of PCCs over FFP include rapid administration of a small volume, with avoidance of volume overload or transfusion reactions (see "Plasma derivatives and recombinant DNA-produced coagulation factors", section on 'PCCs' and "Intraoperative transfusion and administration of clotting factors", section on 'Prothrombin complex concentrates (PCCs)') [73-80]. Its disadvantage is that PCC are missing small amounts of other clotting proteins that FFP contains.
•Cryoprecipitate or fibrinogen concentrate – Fibrinogen concentrate or cryoprecipitate is used to treat hypofibrinogenemia (measured low fibrinogen concentration <150 to 200 mg/dL), or when fibrinogen cannot be measured in a timely fashion as the patient develops clinically significant bleeding [67,81]. . Viscoelastic testing can help guide the decision to treat hypofibrinogenemia (table 2) [67,69]. Low fibrinogen concentration may occur after reperfusion since the ischemic liver graft releases tissue plasminogen activator (tPA) that is washed into the circulation during reperfusion causing ongoing fibrinolysis . (See 'Reperfusion phase' below.)
Since fibrinogen concentrates do not contain FVIII, vWF, and FXIII, these products may have less risk of inducing hypercoagulability than cryoprecipitate . However, cryoprecipitate, which contains FVIII, von Willebrand factor (vWF), FXIII, and fibrinogen, may be used if fibrinogen concentrate is not available. (See "Intraoperative transfusion and administration of clotting factors", section on 'Cryoprecipitate or fibrinogen concentrate' and "Intraoperative transfusion and administration of clotting factors", section on 'Fibrinogen concentrate'.)
•Platelets – We typically hold platelet transfusion until the hepatic artery anastomosis has been completed, and typically avoid such transfusion if the anastomosis is precarious even if platelet count is low. Administration of platelets is an independent predictor of worse outcome after liver transplantation .
Platelet transfusion can usually be avoided during the dissection phase of liver transplantation surgery, even in patients with severe thrombocytopenia, because platelet function is often normal. This is because vWF levels are high and ADAMTS-13 levels are low in patients with end-stage liver disease. Thus, vWF can bind to a smaller amount of activated platelets with a connection that is less likely to be cleaved by ADAMTS-13. Furthermore, platelets that are typically sequestered in the enlarged spleen of patients with portal hypertension are mobilized during bleeding.
Administration of antifibrinolytic agents — We typically administer an antifibrinolytic (either epsilon-aminocaproic acid [EACA] or tranexamic acid [TXA]) typically during the pre-anhepatic phase if there is evidence of hyperfibrinolysis on TEG or ROTEM tests, or diffuse microvascular bleeding is noted [85,86]. (See "Perioperative blood management: Strategies to minimize transfusions", section on 'Antifibrinolytic agents'.)
There is no general consensus and data are limited regarding the utility and safety of prophylactic administration of an antifibrinolytic agent during liver transplantation (see "Liver transplantation: Preanesthetic consultation and preparations", section on 'Disorders of coagulation' and 'Reperfusion phase' below). A 2017 propensity-matched study of patients noted that transfusions of RBC and FFP were reduced in patients receiving TXA compared with those who had no TXA exposure, with no difference in thromboembolic complications after liver transplantation . A 2016 retrospective study also noted that EACA was not associated with an increased incidence of thromboembolic complications compared with no EACA exposure .
●Targeting optimal fluid administration – We typically target a low to normal central venous pressure (CVP) of 7 to 10 mmHg to minimize blood loss, particularly during the dissection phase (see 'Pre-anhepatic (dissection) phase' below) [1,2,4]. CVP generally represents the downstream hydrostatic resistance to blood flow through the liver; the higher the CVP, the more congested the liver which leads to brisk venous bleeding. Higher circulating volume (or over-transfusion) is avoided, as this may worsen bleeding and/or may cause right ventricular (RV) failure. Recognizing that CVP is not a truly reliable indicator of intravascular volume status, we follow directional changes in CVP values that typically indicate changes in portal pressure that affect bleeding. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)
With some surgical techniques, a higher CVP may be necessary to maintain stability. For example, if complete caval clamping is employed, a CVP of 10 to 15 mmHg may be required to maintain hemodynamic stability during the anhepatic phase since a larger proportion of preload is lost compared with the piggyback technique. (See 'Specific surgical techniques' below.)
Some centers advocate a lower volume/lower CVP (ie, <5 mmHg) strategy [36,89-92]. However, this strategy may lead to low intravascular volume status resulting in hypotension and organ hypoperfusion.
●Selection of fluid type – Intraoperative fluid choices include crystalloid or colloid solutions.
•Crystalloid solutions – We use a balanced electrolyte crystalloid solution as maintenance fluid, and we routinely select Plasmalyte or Normosol rather than lactated Ringer solution or 0.9% saline solution .
We generally avoid lactated Ringer solution since lactate accumulation may occur in patients with end-stage liver disease. We generally avoid 0.9% saline, even in patients with hyperkalemia, due to concern for hyperchloremic acidosis. Evidence in patients undergoing kidney transplantation and other major surgical procedures suggests that administration of 0.9% saline (particularly in large volumes) is associated with hyperchloremia, metabolic acidosis, renal vasoconstriction, decreased glomerular filtration rate, and kidney injury [94-103]. (See "Anesthesia for kidney transplantation", section on 'Choosing fluids' and "Intraoperative fluid management", section on 'Crystalloid solutions'.)
Plasmalyte has magnesium rather than calcium (as in lactated Ringer solution), and can therefore be mixed with blood products that contain citrate.
•Colloid solution – We routinely replace known albumin losses with 5% albumin solution (eg, when a large volume of ascites fluid is drained upon entry into the peritoneal cavity) . Patients with documented coagulopathy receive FFP instead.
Data regarding benefits of 5% albumin in this setting are generally scant [105-109], except for those with hepatorenal syndrome or spontaneous bacterial peritonitis [110-112]. However, randomized trials have not demonstrated benefits of albumin compared with crystalloid solutions in other settings [105,107,109].
Point-of-care laboratory testing — In addition to POC tests for Hb and viscoelastic tests of coagulation (see 'Management of anemia' above and 'Management of coagulopathy' above), we employ intraoperative POC measurements of arterial blood gases and pH, arterial lactate, electrolytes, and glucose. Frequent testing and rapid turn-around of these measurements allow detection and correction of abnormalities (eg, acidosis, hyperkalemia, hyponatremia, and hyper- or hypoglycemia) [113,114], which may improve patient stability and graft function.
Immunosuppression — Immunosuppressive drugs should be administered during transplant per institutional protocol. In many centers, steroids are administered during the anhepatic phase so that plasma concentrations are maximal during reperfusion of the donor graft. Calcineurin inhibitors such as tacrolimus and other immunosuppressants such as mycophenolate or azathioprine are typically administered after surgery (eg, on postoperative day one). (See 'Specific considerations for each surgical phase' below and "Liver transplantation in adults: Initial and maintenance immunosuppression".)
SPECIFIC CONSIDERATIONS FOR EACH SURGICAL PHASE — The liver transplantation surgical procedure occurs in four main stages: liver dissection during the pre-anhepatic phase, followed by the anhepatic, reperfusion, and neohepatic phases (table 4). Each phase has unique challenges and goals. Management of fluids, transfusion of blood products, and hemodynamics differ in each stage, and must also be adjusted to accommodate individual patient- and surgery-specific factors.
Pre-anhepatic (dissection) phase — The pre-anhepatic stage begins with surgical incision and includes drainage of ascites fluid and dissection of the native liver from the surrounding tissue in preparation for its removal. Surgical goals include identification of the elements of the porta hepatis fissure in the inferior surface of the liver (eg, bile duct, hepatic artery, portal vein), dissection of the posterior aspect of the liver, and isolation of the vena cava. Anesthetic goals include correction of coagulopathy and maintenance of euvolemia and systemic blood pressure (BP) during drainage of ascites fluid and liver dissection. Challenges include:
●Fluid management – Upon surgical entry into the peritoneum, drainage of a significant volume of ascites fluid may result in severe hypovolemia and hypotension. As drainage occurs, volume is administered (typically 5% albumin solution); the alternative is administration of fresh frozen plasma (FFP) in patients with coagulopathy. Care is taken to avoid low intravascular volume status that may lead to hypotension and organ hypoperfusion. However, fluid overload (or over-transfusion) is also avoided, as this increases portal pressure and worsens bleeding from variceal veins during their dissection. (See 'Fluid management' above.)
●Management of blood loss – Large blood losses may be incurred during dissection around the liver, depending on the severity of coagulopathy and portal hypertension. Notably, significant bleeding may not be immediately obvious (eg, during dissection of the retrohepatic vena cava). Transfusion of red blood cells (RBCs) and other blood products to replace blood loss and correct coagulopathy is used as necessary. (See 'Blood and coagulation management' above.)
●Management of a vasodilatory state – Most patients require vasopressor therapy during this phase because of their chronic vasodilatory state that is typically exacerbated by administration of anesthetic agents, drainage of ascites fluid, and surgical bleeding during liver dissection. (See 'Hemodynamic and vasopressor management' above.)
Anhepatic phase — The anhepatic phase begins when the native liver is removed and ends when the new liver graft is reperfused.
Anesthetic management during this phase is influenced by the recipient's cardiovascular reserve as well as the surgical technique selected (see 'Specific surgical techniques' below). Regardless of these factors. the absence of liver function and hepatic lactate clearance during the anhepatic phase will cause metabolic lactic acidosis with consequent worsening of hyperkalemia.
We measure blood gas and electrolyte values approximately 15 to 20 minutes into the anhepatic phase to detect hyperkalemia and promptly treat potassium levels above 4.0 to 4.5 mEq/L with insulin/glucose. Also, the surgeon is immediately notified about hyperkalemia so that alterations in surgical technique during reperfusion that reduce risk of sudden exacerbation of hyperkalemia may be planned. Blood gas and electrolyte measurements are also repeated frequently (every 15 to 20 minutes) throughout the anhepatic phase. (See 'Hyperkalemia and other metabolic abnormalities' below.)
Specific surgical techniques — The choice of surgical technique depends on patient-specific and donor-specific criteria, as well as surgical and institutional preferences. Studies have not demonstrated the superiority of any one technique [115-117]. The surgeon initiates a trial of the planned surgical technique to confirm hemodynamic stability before irreversible removal of the liver.
The most commonly used techniques are noted below. In some cases, combinations (or variations) of these are employed:
●Complete caval cross-clamping technique – With this technique, the inferior vena cava (IVC) is clamped above and below the liver and commonly resected (figure 2). The donor vena cava is then implanted in place of the resected recipient cava.
This surgical technique greatly impacts recipient hemodynamics. Complete cross-clamping of the IVC results in an acute decrease in right ventricular (RV) preload, cardiac output (CO), and BP. However, administration of large volumes of fluid or blood products to compensate for this sudden loss in preload can result in a circulating volume so large that it can precipitate RV failure during reperfusion (see 'Reperfusion phase' below). In general, complete caval cross-clamping is best tolerated in patients who have extensive collateral portal circulation (varices), while the technique is poorly tolerated in those with acute liver failure or those with low Model for End-stage Liver Disease (MELD) scores (typically patients with hepatocellular cancer) (see "Model for End-stage Liver Disease (MELD)"). With initial clamping of the IVC, it is critically important that the surgeon and anesthesiologist jointly confirm the likelihood that a relatively stable hemodynamic profile can be maintained throughout the anhepatic phase before proceeding with final resection of the IVC and the diseased liver.
Compared with other phases of the procedure, higher doses of vasopressors such as norepinephrine, vasopressin, and possibly epinephrine are typically necessary during this anhepatic phase. In some cases, it is necessary to unclamp the IVC and administer additional fluids before a second attempt at caval cross-clamping is attempted.
Although splanchnic and renal venous stasis also occur during this technique, there is scant evidence of clinically relevant worsening of renal function .
●Piggyback technique – With this technique, a partial clamp is applied to the IVC, thereby excluding the hepatic veins (figure 2), rather than completely cross-clamping the IVC. After resection of the native liver, the donor IVC is sewn on top of the recipient IVC. By avoiding complete caval cross-clamping with these techniques, partial caval blood flow is present and preserves some preload to the right heart throughout the anhepatic phase such that lower volumes of fluid administration are necessary (see 'Fluid management' above). Several variations of the piggyback technique have been developed (eg, end-to-side cavocaval anastomosis or direct anastomosis of donor hepatic veins with the recipient cava. Although these techniques theoretically allow renal venous drainage throughout the anhepatic phase, there is scant evidence for potential benefit (eg, amelioration of renal injury) .
●Temporary portocaval bypass technique – A modification of the piggyback technique is use of a temporary portocaval shunt that drains splanchnic blood into the IVC during the anhepatic phase. Advantages include greater preservation of preload and prevention of excessive engorgement of the bowel compared with use of a piggyback technique without a portocaval shunt. Thus, hemodynamic stability is improved, particularly in patients with severe portal hypertension and/or cardiac comorbidities. However, this modification is not necessary or beneficial in all patients. Disadvantages include a longer duration of surgical time, and potential for complications of the anastomosis.
●Venovenous bypass technique – Venovenous (VV) bypass may be instituted before removal of the liver to compensate for loss of preload during either full or partial clamping of the IVC (figure 3). VV bypass drains blood from the femoral veins and portal vein back into the circulation, either through a cannula inserted into an axillary vein (accessed by cut-down) or via a transcutaneous internal jugular approach guided by transesophageal echocardiography (TEE) .
Advantages of the VV bypass approach include maintenance of excellent hemodynamic stability. Also, it can be used in combination with any other surgical technique (eg, piggyback or caval replacement). Thus, this technique is often selected for patients with severe cardiovascular comorbidities. Disadvantages include increased risk for complications involving venous access (eg, vascular injury, seroma, lymphocele, venous air or thrombotic emboli), increased blood loss, and prolongation of surgical time. For these reasons, most centers no longer routinely employ VV bypass, and the technique has been replaced almost entirely by variations of the piggyback technique, as explained above .
Preparation for reperfusion — In preparation for reperfusion of the donor liver, blood gases and electrolytes should be checked and hyperkalemia is aggressively treated. Ideally a potassium level under 4.0 to 4.5 mEq/L should be achieved prior to reperfusion to minimize potential for severe hyperkalemia and cardiac arrest. (See 'Hyperkalemia and other metabolic abnormalities' below.)
Also, we routinely administer 2 g magnesium sulfate (for its membrane-stabilizing and antidysrhythmic effect)  as an infusion over approximately 10 to 25 minutes during the anhepatic phase in preparation for reperfusion. In one trial, patients receiving 25 mg/kg of magnesium sulfate before reperfusion had lower post-reperfusion arterial lactate levels than those receiving no magnesium .
Reperfusion phase — The reperfusion phase of the donor liver begins with release of the IVC clamp, with sequential reperfusion of the portal vein occurring before or after the hepatic artery.
First, the IVC cross-clamp is released, thereby providing the right heart with increased preload. Typically, BP is increased. However, significant bleeding or a kink at the caval anastomosis site may result in inadequate right heart filling and persistent hypotension.
The portal vein clamp is then released and the donor graft is reperfused. Hypotension as well as pulmonary vasoconstriction may occur due to release of acid byproducts of metabolism, cytokines , endotoxins , and inflammatory mediators , as well as activation of complement cascades . RV dysfunction may occur at this stage due to the sudden increase in preload, pulmonary artery pressure, and RV afterload . This combination of factors may lead to post-reperfusion syndrome.
If the liver has been previously flushed with portal blood to prevent excessive hyperkalemia (see 'Hyperkalemia and other metabolic abnormalities' below), the portal vein may be briefly opened while the IVC is still cross-clamped and part of the caval anastomosis is still open. This maneuver can result in significant blood loss; hence, the anesthesiologist should be ready to administer fluid and/or blood. (See 'Blood and coagulation management' above.)
Most surgeons complete the caval anastomoses, then reperfuse the portal vein first at the beginning of the reperfusion phase, then complete re-anastomosis of the hepatic artery to reperfuse the donor liver with oxygenated arterial blood. However, some centers delay portal vein reperfusion until the hepatic artery anastomosis has been completed so that adequate oxygen delivery to the new liver is ensured. Once anastomosed, acceptable hepatic arterial flow can be confirmed with a Doppler flow meter .
After adequate reperfusion, donor graft liver function is usually re-established. Intraoperative problems with vasodilation and high vasopressor requirements, acidosis and high lactate levels, and coagulopathy and bleeding will generally resolve if donor liver perfusion and function are adequate. However, coagulopathy may persist due to hyperfibrinolysis even if graft function is good. In part, this occurs because of chronic hyperfibrinolysis with decreased hepatic clearance of tissue plasminogen activator (tPA) [58-60] (see "Liver transplantation: Preanesthetic consultation and preparations", section on 'Disorders of coagulation'). Also, accumulation of tPA in the endothelium of the donor liver during the anhepatic phase is then washed into the recipient circulation during reperfusion to worsen hyperfibrinolysis [61,128]. Thus, administration of fibrinogen concentrate or cryoprecipitate is often necessary. (See 'Blood and coagulation management' above.)
Some patients experience post-reperfusion syndrome - defined as a decrease in mean arterial pressure [MAP] >30 percent, occurring within five minutes of reperfusion and lasting longer than one minute. Management is described below. (See 'Post-reperfusion syndrome' below.)
Neohepatic phase — The neohepatic phase begins after the donor liver has been reperfused and continues until the end of the procedure. Stable hemodynamics must be maintained while biliary reconstruction is performed, fastidious surgical hemostasis is achieved, and the abdominal wound is closed. Typically, lactate levels and vasopressor requirements will decrease and hemodynamic stability is present if perfusion and function of the grafted donor are adequate.
Planning for timing of tracheal extubation is necessary as the procedure is being completed. (See 'Early extubation' below.)
MANAGEMENT OF INTRAOPERATIVE COMPLICATIONS — Complications that may occur during and after the reperfusion and neohepatic phases include post-reperfusion syndrome, cardiac arrest, thromboembolism, or persistent delayed graft function.
Post-reperfusion syndrome — Post-reperfusion syndrome with a decrease of more than 30 percent in mean arterial pressure (MAP) that occurs within five minutes of reperfusion occurs in 25 to 50 percent of patients undergoing liver transplantation [22,129-133]. The pulmonary vascular resistance (PVR), pulmonary arterial pressure, and central venous pressure (CVP) increase leading to right ventricular (RV) failure, while systemic vascular resistance (SVR) decreases [4,22,134,135]. In addition to hemodynamic instability, post-reperfusion syndrome may be associated with electrolyte, metabolic, and coagulation abnormalities . Arrhythmias and sudden cardiovascular collapse may occur due to marked hyperkalemia and acidosis. (See 'Cardiac arrest' below.)
Increasing MAP with continuous vasopressor infusions (typically norepinephrine and vasopressin), with additional intermittent boluses of phenylephrine 80 to 120 mcg or epinephrine 10 mcg as needed may prevent development of post-reperfusion syndrome by increasing MAP . Prophylactic administration of atropine or methylene blue has little effect [137,138].
Rapid aggressive treatment is necessary for these manifestations of post-reperfusion syndrome:
●Severe hyperkalemia, recognized by peak T-waves in the ECG (see "Clinical manifestations of hyperkalemia in adults", section on 'ECG changes'), and usually accompanied by severe acidosis, is particularly likely in patients with post-reperfusion syndrome. Treatment is described below. (See 'Hyperkalemia and other metabolic abnormalities' below.)
●Severe hypotension is usually associated with markedly increased CVP and pulmonary artery pressure with decreased heart rate, resulting in right heart failure . Treatment includes boluses of epinephrine and phenylephrine, in addition to continuing infusion of higher doses of norepinephrine (and often vasopressin) (table 1). If hemodynamic stability is not rapidly achieved, the surgeon can reclamp the portal vein.
Post-reperfusion syndrome is associated with cardiac arrest, postoperative renal failure, and decreased 15-day survival [129-133,139]. It occurs more commonly in patients who did not have a portocaval shunt, or if there is a prolonged duration of cold ischemia time, marginal donor graft, or organ size mismatch.
Hyperkalemia and other metabolic abnormalities — Although preoperative electrolyte abnormalities are common in patients with end-stage liver disease and are typically corrected during the dissection phase of liver transplantation, exacerbations may occur at any stage of the procedure.
●Hyperkalemia – Severe exacerbations of hyperkalemia are particularly common during reperfusion, and must be aggressively treated:
•Any potassium level above 4.5 to 5.0 mEq/L is treated with insulin (and dextrose depending on glucose levels), furosemide, and calcium. (See "Anesthesia for kidney transplantation", section on 'Management of hyperkalemia'.)
Calcium is typically generously administered in patients requiring massive transfusion to compensate for hypocalcemia caused by the citrate anticoagulant in fresh frozen plasma (FFP) and red blood cell (RBC) transfusions (see "Massive blood transfusion", section on 'Hypocalcemia from citrate toxicity') . Either calcium chloride or calcium gluconate may be administered since these agents have similar pharmacokinetic profiles (even in the absence of liver function) . Calcium chloride should be given through a central venous catheter (CVC) to minimize risk of tissue necrosis if extravasation occurs.
•Washing RBCs as part of the blood salvage process removes potassium. (See "Surgical blood conservation: Blood salvage".)
•The surgical team is immediately notified if hyperkalemia is present. In such cases, the team may elect to leave the caval anastomosis unfinished after completion of the portal anastomosis, so that the donor graft can be flushed (by temporarily unclamping the portal vein and draining the blood into the field through the hole in the caval anastomosis). This reduces the risk of potentially catastrophic hyperkalemia during reperfusion. Advance planning is necessary to carry out these maneuvers. (See 'Specific surgical techniques' above.)
•In rare cases, intraoperative continuous renal replacement therapy (CRRT) may be necessary to treat hyperkalemia. However, CRRT is a very slow and inefficient way to remove potassium. (See "Liver transplantation: Preanesthetic consultation and preparations", section on 'Use of continuous renal replacement therapy'.)
●Acidosis – Severe acidosis may also be present during reperfusion due to acid load entering the systemic circulation after release of the portal vein cross-clamp, as well as increased arterial partial pressure of carbon dioxide (PaCO2) . Sodium bicarbonate 1 to 2 mEq/kg may be administered (in incremental intravenous [IV] boluses or as an infusion over 5 to 10 minutes) to treat severe metabolic acidosis (ie, pH <7.1 and serum bicarbonate ≤6 mEq/L) that would otherwise limit the effectiveness of vasopressor and inotropic support . The dose is repeated after 30 minutes if pH remains <7.1. Notably, administration of sodium bicarbonate may cause a shift of the oxyhemoglobin curve to the left with worsening of reperfusion injury [143,144]. Also, administration of bicarbonate may cause overly rapid correction of hyponatremia, as noted below.
●Hyponatremia – Hyponatremia is common in liver failure patients with cirrhosis, particularly if marked ascites is present (see "Hyponatremia in patients with cirrhosis"). Too rapid correction of hyponatremia is avoided, as this is associated with risk for neurologic complications and pontine myelinolysis. Correction may be too rapid when:
•FFP is administered in high volumes, since FFP contains a high concentration of sodium.
•CRRT is employed. To avoid rapid correction of hyponatremia during CRRT, it may be necessary in rare cases to add dextrose to the dialysate fluid to lower its sodium concentration or add an IV infusion of D5W. Most dialysate fluids contain 140 mEq/L of sodium, and the blood concentration will rapidly equilibrate with this dialysate. (See "Liver transplantation: Preanesthetic consultation and preparations", section on 'Use of continuous renal replacement therapy'.)
●Hyperglycemia or hypoglycemia
•Hyperglycemia – Although precise target glucose values have not been established, we typically treat hyperglycemia with a continuous infusion of regular insulin if blood glucose is >180 mg/dL (see "Perioperative management of blood glucose in adults with diabetes mellitus", section on 'IV insulin infusion'). Hyperglycemia is common during liver transplantation due to administration of steroids for immunosuppression and the use of catecholamine vasoactive agents. (See 'Immunosuppression' above and 'Hemodynamic and vasopressor management' above.)
•Hypoglycemia – Hypoglycemia is readily treated with iv dextrose if it occurs. However, since hypoglycemia is a late sign of acute liver failure, it is rare during liver transplantation . (See "Perioperative management of blood glucose in adults with diabetes mellitus", section on 'Avoidance of hypoglycemia'.)
Thromboembolism — Liver disease causes an imbalance of pro- and anticoagulant factors that may result in hypercoagulability with thromboembolism and coagulopathy with bleeding, either alone or concomitant. (see "Liver transplantation: Preanesthetic consultation and preparations", section on 'Disorders of coagulation'). If a thrombus is detected, treatment depends on its size, location, and consequent hemodynamic effects. Large symptomatic thromboembolic complication are potentially fatal, and are typically treated with tissue-type plasminogen activator (tPA) [146,147]. Successful treatment of smaller emboli may be achieved with a heparin bolus .
If pulmonary or intracardiac thromboembolus is suspected, the diagnosis should be rapidly confirmed with transesophageal echocardiography (TEE) [9,23,33]. A "flat-line," thromboelastogram (TEG) occurring within five minutes of initiating reperfusion predicts pulmonary thromboembolic complications (figure 1) . Such a "flat-line," TEG probably indicates profound hyperfibrinolysis, either due to disseminated intravascular coagulation or formation of large venous clots that consume fibrin.
Cardiac arrest — Cardiac arrest may occur at any time during liver transplantation, but is most common shortly after reperfusion (see 'Reperfusion phase' above). Cardiopulmonary resuscitation (CPR) should commence immediately, either by direct cardiac massage through an incision in the diaphragm or with external chest compressions (see "Intraoperative advanced cardiac life support (ACLS)", section on 'Initial resuscitation') . Potential causes are quickly assessed and treated (see 'Hyperkalemia and other metabolic abnormalities' above and 'Thromboembolism' above). If adequate CPR does not result in return of sustained spontaneous circulation, then venoarterial extracorporeal membrane oxygenation (VA ECMO) may be initiated to restore perfusion and allow time for recovery . (See "Extracorporeal life support in adults in the intensive care unit: Overview" and "Extracorporeal life support in adults in the intensive care unit: The role of transesophageal echocardiography (TEE)".)
In a single-center retrospective study of 1238 patients, 5.5 percent suffered intraoperative cardiac arrest, with 90 percent occurring during the neohepatic phase in patients with post-reperfusion syndrome . The most common direct causes of cardiac arrest were hyperkalemia and pulmonary thromboembolism.
CONSIDERATIONS IN THE IMMEDIATE POSTOPERATIVE PERIOD
Early extubation — Immediate extubation in the operating room, or early extubation a few hours after surgery, has become more common for hemodynamically stable patients [152,153]. However, early extubation is not suitable for all liver transplant recipients. Examples include those with severe preoperative comorbidities, intraoperative complications, concerns regarding poor graft quality, or persistent bleeding that may require early (<36 hours) re-exploration. (See 'Management of intraoperative complications' above.)
Postoperative pain management — Optimal postoperative pain management is required, as in any major abdominal surgical procedure. The right subcostal incision is often most painful. We typically administer systemic opioids with a patient-controlled analgesia technique.
Some centers also administer nonopioid analgesics such as ketamine, clonidine, acetaminophen, and nonsteroidal antiinflammatory drugs (NSAIDs) to reduce opioid requirements [4,154]. A few use thoracic epidural analgesia in patients without severe coagulopathy , or a subcostal transversus abdominis plane , or erector spinae block. (See "Continuous epidural analgesia for postoperative pain: Technique and management" and "Transversus abdominis plane (TAP) blocks procedure guide" and "Erector spinae plane block procedure guide".)
Early postoperative complications — In addition to the intraoperative complications described above (see 'Management of intraoperative complications' above), problems that may occur in the early postoperative period include persistent bleeding or graft dysfunction.
Persistent bleeding — Persistent bleeding due to persistent coagulopathy may occur at the end of surgery as a result of early graft dysfunction, or less commonly due to inadequate surgical hemostasis. Viscoelastic testing may be used to differentiate between these causes and guide transfusion of coagulation factors (figure 1) (see 'Management of coagulopathy' above). If bleeding persists after transfusion of a large volume of blood products, the surgical team may elect to pack the abdomen with surgical sponges and close the wound. Once coagulopathy has been corrected, the patient can return to the operating room (typically within 24 hours) for removal of the packing and completion of any additional surgical procedures. This "damage control," approach has been used in approximately 8 percent of liver transplantation cases, and can be initiated either before or after completion of the biliary anastomosis [157,158]. In these reports, intermediate- and long-term graft and patient survival was comparable to patients who did not need such a damage control approach.
Persistent delayed graft function — Persistent delayed graft dysfunction or worsening graft failure manifests as increasing levels of arterial lactate , and worsening coagulopathy within a short time after reperfusion. These early signs of donor graft dysfunction necessitate prompt rapid evaluation for correctable causes such as complications of the hepatic artery (or portal vein) anastomosis or low cardiac output (CO) state with decreased hepatic arterial perfusion. In rare cases of a nonfunctioning donor graft, relisting the patient for repeat transplantation offers the best chance for survival .
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Liver transplantation".)
SUMMARY AND RECOMMENDATIONS
●Reliable large bore venous access is necessary for administration of intravenous (IV) fluids, blood products, and vasopressors. We typically insert a central venous catheter (CVC) into an internal jugular vein before surgical incision. In many centers, an additional peripheral large-bore rapid infusion catheter is also inserted. (See 'Intravascular access' above.)
●Cardiovascular monitoring routinely includes two intra-arterial catheters, CVC to monitor central venous pressure (CVP), pulmonary artery catheter to monitor cardiac output (CO) and pulmonary artery pressure (PAP), as well as transesophageal echocardiography (TEE) to monitor hemodynamics and to diagnose causes of hemodynamic instability. (See 'Monitoring considerations' above.)
●Rapid sequence anesthetic induction and endotracheal intubation is usually employed because of inadequate time for fasting and/or increased intra-abdominal pressure due to moderate or severe ascites. Administration of vasopressors to maintain hemodynamic stability is typically necessary during induction. Either inhalation or IV agents may be used to maintain general anesthesia. (See 'Induction of general anesthesia' above and 'Maintenance of general anesthesia' above.)
●We maintain mean arterial pressure (MAP) ≥65 to 75 mmHg throughout all phases of liver transplant procedures. A higher target may be selected for patients with preexisting hypertension. Most patients require vasopressor therapy such as norepinephrine (and additionally vasopressin) during various phases of the transplant procedure to maintain the target MAP (table 1). (See 'Hemodynamic and vasopressor management' above.)
●Transfusions of red blood cells (RBCs) and other blood products including fresh frozen plasma (FFP) or prothrombin complex concentrate (PCC), cryoprecipitate or fibrinogen concentrate, and platelets are usually necessary during liver transplantation surgery. Intraoperative blood salvage using a cell saver system is typically employed to avoid or minimize allogeneic RBC transfusion. Intraoperative point-of care (POC) testing for anemia and coagulopathy allows for rational decision-making regarding transfusions. (See 'Blood and coagulation management' above.)
●We suggest a low to normal CVP target of 7 to 10 mmHg (Grade 2C). We suggest administration of the balanced electrolyte crystalloid solution Plasmalyte or Normosol as maintenance fluid (Grade 2C). We replace known albumin losses (eg, when a large volume of ascites fluid is drained upon entering the peritoneal cavity) with 5% albumin solution. Patients with documented coagulopathy receive FFP instead. (See 'Fluid management' above.)
●Intraoperative POC laboratory testing includes measurement of arterial blood gases and pH, arterial lactate, electrolytes, and glucose. Frequent testing and rapid turn-around of these measurements allow detection and correction of abnormalities (eg, hyperkalemia, acidosis, hyponatremia, hypoglycemia, hyperglycemia). (See 'Point-of-care laboratory testing' above.)
●Specific considerations for each phase of the liver transplantation procedure are noted above (see 'Specific considerations for each surgical phase' above):
•The pre-anhepatic stage includes the initial incision, drainage of ascites, and surgical dissection of the native liver in preparation for its removal. (See 'Pre-anhepatic (dissection) phase' above.)
•The anhepatic phase begins when the native liver is removed and ends when the new graft is reperfused. The surgeon initiates a trial of the selected surgical technique to confirm hemodynamic stability before irreversibly removing the liver. (See 'Anhepatic phase' above and 'Specific surgical techniques' above.)
•In preparation for reperfusion of the donor liver, blood gases and electrolytes should be checked and hyperkalemia is aggressively treated. We suggest administration of 2 g magnesium sulfate as an infusion over approximately 10 to 25 minutes in preparation for reperfusion (Grade 2C). (See 'Anhepatic phase' above and 'Preparation for reperfusion' above.)
•The reperfusion phase of the donor liver begins with release of the IVC clamp, with sequential reperfusion of the portal vein and hepatic artery. (See 'Reperfusion phase' above.)
•The neohepatic phase begins after the donor liver has been reperfused, and includes biliary reconstruction, fastidious surgical hemostasis, closure or the abdominal wound, and planning for tracheal extubation. If perfusion and function of the grafted donor are adequate, lactate levels and vasopressor requirements will decrease. (See 'Neohepatic phase' above.)
●Severe intraoperative complications requiring rapid treatment may occur. These include:
•Post-reperfusion syndrome (a decrease in MAP >30 percent, occurring within five minutes of reperfusion and lasting longer than one minute) may result in right heart failure, or severe hypotension or hyperkalemia. (See 'Post-reperfusion syndrome' above.)
•Severe exacerbations of hyperkalemia and acidosis are particularly likely during reperfusion and must be aggressively treated. Other metabolic abnormalities include hyponatremia and hypoglycemia or hyperglycemia. (See 'Hyperkalemia and other metabolic abnormalities' above.)
•Diagnosis of suspected pulmonary or intracardiac thromboembolus is rapidly confirmed with TEE. Large symptomatic potentially fatal thromboembolic complications are often treated with tissue-type plasminogen activator (tPA) while a heparin bolus may adequately treat smaller emboli. (See 'Thromboembolism' above.)
•Cardiac arrest most commonly occurs shortly after reperfusion due to hyperkalemia or thromboembolic complications. In some cases, venoarterial extracorporeal membrane oxygenation (VA ECMO) may be initiated. (See 'Cardiac arrest' above.)
●For postoperative pain management, we typically administer systemic opioids with a patient-controlled analgesia technique. Some centers use nonopioid analgesics such as ketamine, clonidine, acetaminophen, and nonsteroidal antiinflammatory drugs (NSAIDs) or a regional anesthetic technique such as subcostal transversus abdominis plane block to reduce opioid requirements. (See 'Postoperative pain management' above.)
●Postoperative complications may include:
•Persistent bleeding due to persistent coagulopathy as a result of early graft dysfunction or inadequate surgical hemostasis. Viscoelastic testing may be used to differentiate between these causes (figure 1). In some cases, the abdomen is packed with sponges and the wound is closed, with planned completion of the procedure after approximately 24 hours when coagulopathy has been corrected. (See 'Persistent bleeding' above.)
•Persistent delayed graft dysfunction or worsening graft failure with increasing lactate levels and vasopressor requirements, and worsening coagulopathy. Correctable causes are sought (eg, complications of the portal vein or hepatic artery anastomosis, low CO state with decreased hepatic arterial perfusion). (See 'Persistent delayed graft function' above.)
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