Cardiovascular System

Hyperdynamic circulation, cardiomyopathy, and CAD are common clinical problems that impact postoperative outcomes in orthotopic liver transplantation (OLT) candidates (Fouad et al, 2009).

Pulmonary System

As many as 70% of patients with chronic liver disease (CLD) suffer from respiratory problems, that manifest as impaired respiratory mechanics and gas exchange (Kim et al, 2009). Most pulmonary diseases are independent from the liver disease but are in some instances related to liver disease (e.g., α₁-antitrypsin deficiency and cystic fibrosis) (Yeshua et al, 2009). Pulmonary evaluation includes history and physical examination, radiologic studies, arterial blood gas, and pulmonary function tests. Right-heart catheterization is indicated when clinical or ECG evidence suggests pulmonary hypertension.

Hemostasis in End-Stage Liver Disease

The liver synthesizes most of the factors involved in clot formation and, equally importantly, factors opposing clot formation or mediating its lysis. The traditional concept that patients with advanced liver disease are hypocoagulable has been challenged. The current view emphasizes complex disturbances of platelet function, procoagulant, anticoagulant, and fibrinolytic pathways that result in rebalancing of the hemostatic system (Senzolo et al, 2006). The net effect may be a hypocoagulable or hypercoagulable state with a tendency for bleeding or thromboembolism (Warnaar et al, 2008b). Understanding the hemostatic system in ESLD is essential to perioperative coagulation management and optimization of blood product transfusion practices, which are directly related to morbidity and mortality in liver transplantation (de Boer et al, 2008; Massicotte et al, 2005).

Deficiency in primary hemostasis is due to quantitative and qualitative platelet changes (Pereboom et al, 2008). Mild to moderate thrombocytopenia is common. Causes are splenomegalic platelet sequestration in portal hypertension, impaired megakaryocytopoiesis as a result of reduced production of thrombopoietin by the cirrhotic liver, folic acid deficiency in alcoholic cirrhosis or acute hepatitis C infection, and reduced platelet half-life related to autoantibodies (Lisman & Leebeek, 2007; Senzolo et al, 2006). Evidence for impaired platelet aggregation and adhesion in cirrhosis is controversial. The proposed mechanisms are complex and multifactorial, including the important role of two potent endothelium-derived platelet inhibitors, nitric oxide and prostacyclin. Contrary to this, more recent work suggests that the functional capacity of platelets in cirrhotic patients may be normal when platelet number and hematocrit are normalized (Lisman & Leebeek, 2007; Tripodi et al, 2007), suggesting that the main defect in primary hemostasis is thrombocytopenia. An important compensatory mechanism for the overall deficient platelet function in cirrhosis is an increase in endothelium-synthesized von Willebrand factor (vWf). The markedly upregulated vWf promotes adhesion of platelets to injured vasculature and seems to be more effective than plasma from healthy volunteers (Lisman & Leebeek, 2007).

Hepatocytes synthesize all procoagulant factors except vWF, which is synthesized by the endothelium. Factor VIII is synthesized by hepatocytes but also by nonhepatic sinusoidal endothelial cells. Reduced levels of coagulation factors are observed in acute and chronic liver disease. Several factors—II, VII, IX, and X—require vitamin K as an essential cofactor and exist in plasma as inactive precursors when vitamin K is deficient as a result of decreased absorption (cholestasis) or antagonism (warfarin). In acute liver failure (ALF), plasma concentrations of coagulation factors with the shortest half-life (factor VII, 4 to 6 hours; factor V, 12 hours) decrease first, followed by those with a longer half-life. An exception are factors VIII and vWf, which may be elevated in chronic and acute liver disease because of inflammatory cytokine-mediated upregulated extrahepatic production and because of relative sparing as a result of inhibition of thrombin by antithrombin III. Fibrinogen is usually well preserved, and decreased fibrinogen is a mark of advanced cirrhosis or ALF; however, even when levels are normal, fibrinogen is often functionally aberrant because of impaired fibrin polymerization and results in an abnormal thrombin time (TT) despite normal international normalized ratio (INR) and partial thromboplastin time (PTT).

The deficiency in procoagulant factors is, at least in part, offset by decreased production of anticoagulants, including proteins C and S, antithrombin III, and heparin cofactor II. Proteins C and S are vitamin K dependent and may be deficient in cholestatic disease, and although genetic deficiency of these two proteins is rare, such deficiency is found in both Budd-Chiari syndrome and portal vein thrombosis. Antithrombin III is synthesized by hepatocytes and endothelium, deficiencies are usually mild, and thromboembolic complications rare.

All proteins involved in fibrinolysis are synthesized by the liver except tissue plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1). Consequently, reduced levels of liver-synthesized factors—plasminogen, plasmin inhibitor, thrombin activatable fibrinolysis inhibitor (TAFI), and factor XIII—are found in both acute and chronic liver failure. Cirrhosis is classically associated with hyperfibrinolysis, whereas patients in ALF may have hypofibrinolysis as a result of increased production of PAI-1. The recent expert viewpoint is contrary to the traditionally held view and emphasizes that the existing in vitro evidence of hyperfibrinolysis in cirrhosis is weak (Lisman & Leebeek, 2007). Increased levels of fibrinogen degradation indicators—d-dimers, plasmin-antiplasmin and thrombin-antithrombin complexes, thrombin fragment F1+2—could be explained by their delayed clearance by the diseased liver.

Coagulation tests, such as the prothrombin time (PT) and activated partial thromboplastin time (aPTT), are used to assess the severity of synthetic dysfunction, and PT-INR is a part of the Child-Turcotte-Pugh (CTP) and Model for End-Stage Liver Disease (MELD) prognostic indexes (Ng, 2009). As tests of in vivo coagulation function, PT-INR and PTT are conceptually deficient because they measure only the procoagulant pathway and ignore the anticoagulant function. This inadequacy is best illustrated by the observation that when the (prolonged) PT is modified by including thrombomodulin to allow full activation of protein C, the thrombin generation in cirrhotic patients is close to normal (Tripodi et al, 2005). This may in part explain why PT-INR and PTT are poor predictors of bleeding in cirrhosis and in liver transplantation (Massicotte et al, 2008). Thromboelastogram (TEG; Haemoscope Corp., Niles, IL) and rotation thromboelastometry (ROTEM; Pentapharm, Munich, Germany) have the advantage of assaying whole-blood clot formation and lysis, including the platelet contribution, but these assays do not incorporate the endothelial component (see Intraoperative Monitoring, below). Importantly, these assays allow easy recognition of hypercoagulable states (Fig. 97B.1A).

FIGURE 97B.1 Intraoperative transesophageal echocardiography (TEE) in a patient with hepatopulmonary syndrome and intrapulmonary shunting demonstrates a positive bubble study. A, Midesophageal bicaval view. B, Bolus of contrast injectate (agitated saline-blood mixture) is visible entering the right atrium via the superior vena cava (SVC) following an injection through the central venous port. C, Several heartbeats later, the injectate is present in the left atrium (LA), indicating transpulmonary passage. RA, right atrium; IS, interatrial septum; IVC, inferior vena cava.

Renal System

Renal failure confers increased risk of death to cirrhotic patients, both while on the transplant waiting list and after liver transplantation. Implementation of the MELD score in 2002 (Moreau et al, 2003) has prioritized patients with renal failure waiting for a liver transplant, resulting in reduced overall mortality on the transplant list (Ojo, 2009).

Hepatorenal syndrome (HRS) is a specific type of renal failure in patients with cirrhosis, ALF, or alcoholic hepatitis. It is marked by functional renal vasoconstriction and a severe reduction in glomerular filtration rate (GFR <30 mL/min) but only minimal renal histologic abnormalities (Gines & Schrier, 2008). The primary pathophysiologic process in HRS is a circulatory disturbance: portal hypertension facilitates translocation of bacteria from the intestinal lumen into the mesenteric lymph nodes and induces production of inflammatory cytokines and local vasodilators, such as nitric oxide, carbon monoxide, and endogenous cannabinoids. Resulting splanchnic vasodilatation decreases the overall systemic vascular resistance and activates a number of compensatory mechanisms. The initial response is hyperdynamic and comprises tachycardia, increased cardiac output, low SVR, and relative hypotension.

With progression of cirrhosis, sympathetic and rennin-angiotensin vasoconstrictor systems are activated that temporarily maintain arterial blood pressure, but they also cause renal vasoconstriction and hypoperfusion. Activation of nonosmotic hypersecretion of arginine vasopressin, aimed at preserving circulatory volume, results in retention of solute-free water with attendant hyponatremia, edema, and ascites. HRS is almost invariably associated with ascites and rarely develops in its absence (see Chapter 74). HRS is classified into one of two types: HRS 1 is characterized by a rapid decline in renal function reflected in doubling of serum creatinine (SCr) to above 2.5 mg/dL over a 2-week period; this type of HRS has a particularly ominous clinical course, leading to multiorgan dysfunction that affects the heart, brain, and other organs. HRS 2 has a more benign, slowly progressive course. It is manifested by a milder elevation of SCr (1.5 to 2.5 mg/dL) and refractory ascites. Onset of HRS is often triggered by a discrete event, such as spontaneous bacterial peritonitis, use of nonsteroidal antiinflammatory drugs (NSAIDs), or hypovolemia as a result of diuretic use, gastrointestinal (GI) bleeding, or fluid losses.

It is important to recognize that HRS may be superimposed on a chronic disease, such as glomerulonephritis as a result of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection, interstitial nephritis as a side effect of certain drugs, or nephropathy resulting from diabetes or CLD. Diagnosis of HRS is of great prognostic significance: median survival for HRS 1 is 1 month; for HRS 2, it is 6 months.

Measurement of SCr remains the primary test of renal function despite its well-known limitations. By consensus, SCr above 1.5 mg/dL (133 µmol/L) defines renal insufficiency in cirrhosis (Gines & Schrier, 2008; Salerno et al, 2007). GFR and creatinine clearance are more accurate but less practical tests when repeated assessments are needed. Other tests measure serum and urinary electrolytes, fractional sodium excretion (FENa), albumin, osmolarity, sediment, and biologic markers. Specific diagnostic tests for HRS do not exist, rather diagnosis is based on the presence of liver disease, a precipitating factor, and FENa less than 1%, signifying preserved tubular reabsorption; however, the latter test is invalidated by the use of diuretics.

General treatment measures are aimed at 1) preventing infection, in particular subacute bacterial peritonitis; 2) maintaining adequate intravascular volume; and 3) avoiding nephrotoxic agents. Circulatory volume losses, often the result of large-volume paracentesis or a GI bleed, are best treated with albumin or, if indicated, by blood products and not with crystalloids, to avoid retention of solute-free water.

The main pharmacologic approach utilizes vasoconstrictors, including a selective vasopressin V1 receptor agonist, such as terlipressin, or α-adrenergic agonists, such as norepinephrine and midodrine. Vasoconstrictors in conjunction with albumin are only modestly beneficial but are the best medical therapy currently available. Two recent studies showed a marked improvement in renal function in 40% of patients treated with terlipressin and albumin compared with controls treated with albumin alone (Martin-Liahi et al, 2008; Sanyal et al, 2008). Although the overall survival in the treatment group was not better than in the control group, the probability of 3-month survival in patients who responded with improved renal function was significantly higher (58% vs. 15%) than in nonresponders (Martin-Liahi et al, 2008); however, organ ischemia is a concerning side effect of vasoconstrictor administration.

Placement of a TIPS improves renal function and GFR and reduces sympathetic and renin-angiotensin-aldosterone axis activation in about 60% of patients (Cardenas & Gines, 2009; see Chapter 76E). TIPS is less applicable in HRS 1 as a result of severe liver disease, but it may delay progression of HRS 2 to HRS 1. No advantage in survival has been demonstrated in patients with refractory ascites treated by TIPS compared with repeated paracentesis and intravascular volume replacement with albumin.

Renal replacement therapy (RRT) offers a bridge to transplant, but the optimal RRT method in HRS and the benefit to patient outcomes are not known (Gines & Schrier, 2009). Continuous venovenous hemodialysis (CVVHD) seems to be hemodynamically the most favorable form of RRT (Davenport, 2009). CVVHD can be used to effectively control intravascular volume, pH levels, and solutes (Na, K, SCr, urea, ammonia); in addition, it corrects sodium in a time-controlled fashion, which is particularly relevant to minimize the risk of pontine demyelination in patients with hyponatremia.

Liver transplantation is the treatment of choice for patients with cirrhosis and HRS (Cardenas & Gines, 2009; see Chapter 97A). About 90% of patients with HRS recover kidney function after successful liver transplantation. The remaining 10% do not recover their kidney function and require prolonged RRT and eventual kidney transplantation. When the cause of renal failure in cirrhosis is HRS, the best predictor of need for a combined liver-kidney transplant is pretransplantation RRT for longer than 8 weeks.

Central Nervous System

Hepatic encephalopathy (HE) is a progressive but potentially reversible metabolic disorder of the central nervous system (CNS), and it is associated with variable degrees of brain edema. HE is an overt manifestation of cirrhosis in up to 45% of patients, and it is a defining sign and main cause of death in ALF (Eroglu et al, 2009). The World Congress of Gastroenterology recognizes three classifications of HE based on the etiology (Ferenci et al, 2002): type A is associated with ALF, type B with TIPS, and type C with cirrhosis. Based on the severity of neurologic impairment, HE ranges from normal (grade 0) to mildly impaired cognitive and neuromuscular function (grade 1), progressive lethargy (grade 2), confusion with muscle rigidity or clonus (grade 3), to coma and brain death (grade 4). Although presence and severity of HE has prognostic and therapeutic significance in cirrhosis and ALF, it is not a part of the MELD score.

The pathophysiology of HE is complex and incompletely understood. Multiple putative mediators have been implicated that include ammonia, endogenous benzodiazepine-like or γ-aminobutyric acidlike agonists, reactive oxygen species, inflammatory cytokines, hyponatremia, and manganese. The exact pathogenesis of cerebral edema remains controversial, but good evidence supports the role of ammonia, which promotes astrocyte and neuron swelling by increasing intracellular glutamine content. Transported to the mitochondria, glutamine contributes to production of reactive oxygen species and activation of mitochondrial transition permeability pore and various kinases, resulting in cellular swelling. Increased ammonia levels have been shown to alter cerebral blood flow and brain glucose utilization (Bjerring et al, 2009; Sundaram et al, 2009). High arterial and brain levels of ammonia in ALF correlate well with cerebral edema and increased ICP, with consequent high risk of mortality from brain herniation and hypoxia (Wendon et al, 2008).

HE in cirrhosis features slow onset, a progressive course, and only partial responsiveness to therapy. Significant cerebral edema typically does not develop, and a precipitating event—such as infection, excessive dietary protein, dehydration, or GI bleeding—can be often identified. TIPS is a known risk factor and is associated with 30% of new or worsening encephalopathy (see Chapter 76E). In addition to correction of any precipitating factors, treatment includes nonabsorbable disaccharides, which reduce the intestinal production and absorption of ammonia; antibiotics that target urease-producing bacteria; ornithine and acarbose; benzodiazepine receptor antagonists; and probiotics.

The hallmarks of HE in ALF are cerebral edema and increased intracranial pressure (ICP). Both are life-threatening complications of grade 3 and 4 encephalopathy. Treatment includes a number of general and specific interventions (Table 97B.1) aimed at promoting cerebral perfusion pressure (CPP) above 60 mm Hg; this is achieved by maintaining mean arterial pressure (MAP) and reducing ICP to below 20 to 25 mm Hg by reducing brain edema. Grade 3 or 4 HE requires endotracheal intubation for airway protection. Mild hyperventilation temporarily relieves brain hyperemia, but prolonged hyperventilation is not beneficial and may cause CNS ischemia. Mannitol is effective in reducing ICP in the short term, but its prophylactic use is not recommended. Recent evidence demonstrates that N-acetylcysteine treatment may also prolong transplant-free survival in ALF unrelated to paracetamol/acetaminophen toxicity (Lee et al, 2007).

Table 97B.1 Management of Encephalopathy and Elevated Intracranial Pressure in Acute Liver Failure

CVVHD, continuous venovenous hemodialysis; ICP, intracranial pressure

The role of ICP monitoring is controversial, as ICP monitor placement is associated with high risk of bleeding in this patient population, and no data exist to support its role in improving patient outcomes. The Acute Liver Failure Study Group recommends this intervention only for liver transplant candidates but recognizes regional practice differences (Stravitz et al, 2007). An attractive, noninvasive alternative to ICP monitors is transcranial Doppler (TCD) sonography. By measuring blood flow velocities in middle and anterior cerebral arteries and calculating resistance and pulsatility indexes, TCD allows serial estimates of cerebral blood flow in the setting of impaired autoregulation and developing brain edema (Bhatia & Gupta, 2007). In a small series of ALF patients, confirmation of adequate cerebral blood flow by TCD was successfully used as a basis to proceed with OLT (Bindi et al, 2008). Intraoperative use of TCD in OLT has not been reported.

Mild to moderate hypothermia (32° C to 35° C) is an emerging therapeutic modality. Hypothermia reduces brain ammonia and cytokine levels and in part restores cerebrovascular autoregulation and brain glucose metabolism. Although experimental evidence provides a strong rationale, only limited clinical data on efficacy and safety of hypothermia in humans in ALF are available, and future studies are warranted (Stravitz et al, 2009).

Hemodynamic Management

Hemodynamic management is a cornerstone in the perioperative care of liver transplant patients, but no consensus has been reached on the standards of hemodynamic monitoring (Claus-Georg & De Wolf, 2008). Continuous invasive arterial pressure monitoring may be the only ubiquitously used hemodynamic monitor in liver transplantation. When measured at the most common site, the radial artery, peripheral arterial pressure may underestimate the true aortic pressure, particularly during periods of hypotension. A femoral arterial line reflects central aortic pressure with higher fidelity and consistently records higher systolic pressures than the radial artery. The difference between the femoral and the arterial pressure waveform is particularly pronounced after graft reperfusion or when high doses of vasopressors are used (De Wolf, 2006; Shin et al, 2007). Because of this discrepancy, and because of the need for frequent arterial blood sampling, some centers routinely use both femoral and radial arterial lines.

The pulmonary artery catheter (PAC, see Chapter 22) has long been the mainstay of hemodynamic monitoring in liver transplantation (De Wolf et al, 1993); however, the clinical utility of PACs has recently been questioned because of criticisms that its invasiveness is not justified by improved outcomes (Sandham et al, 2003; Wheeler et al, 2006) and that measured pressures are not good estimates of ventricular preload (Kumar et al, 2004). Although a number of less invasive technologies have emerged, resulting in a decrease in their use, PACs are still advocated by many for OLT (Della Rocca et al, 2008; De Wolf, 2008; Pinsky, 2006), and the ability of PACs to continuously display pulmonary artery pressures is particularly advantageous when managing patients with portopulmonary hypertension. Transesophageal echocardiography (TEE) provides different but complementary information to that provided by PACs (see below), and concurrent use of both devices is considered superior (De Wolf & Aggarwal, 2008). A notable shortcoming of PACs in OLT is the inaccuracy of thermodilution cardiac output in the period following liver reperfusion because of postreperfusion hypothermia and subsequent instability of central temperature.

Newer, less invasive hemodynamic monitors for OLT have been introduced. The PiCCO system (Pulsion Medical Systems, Munich, Germany) combines transpulmonary thermodilution and arterial pressure contour analysis, and it provides continuous cardiac output in alignment with PAC thermodilution and a number of indices of preload that include global end-diastolic volume (GEDV) and intrathoracic blood volume (ITBV), which agree better with cardiac index than filling pressures (Della Rocca et al, 2002a, 2002b). PiCCO requires central venous and femoral or brachial arterial access, which arguably is not much less invasive than the PAC. The LiDCO device (LiDCO Group, London, UK) estimates cardiac output based on the peripheral arterial pressure waveform pulse power analysis after a lithium dilution calibration, and it has been used successfully in patients recovering from liver transplantation in the ICU (Costa et al, 2008). A device that estimates cardiac output based on the arterial pressure waveform without need for calibration, Flo-Trac/Vigileo (Edwards Lifesciences, Irvine, CA), did not perform well intraoperatively during OLT (Biais et al, 2008; Biancofiore et al, 2009).

The accuracy of all arterial pressure–based cardiac output monitors depends critically on accurate determination of arterial compliance, which changes rapidly in liver transplantation, particularly at reperfusion or clamping of major vessels; and because it cannot be readily measured, the assumed value of vascular compliance used in the algorithms of the devices to calculate cardiac output may lead to inaccurate calculations. The inaccuracy may be mitigated by repeated calibrations with the LiDCO or PiCCO.

Cardiac output determined by a novel suprasternal ultrasound cardiac output monitor (USCOM Pty, Coffs Harbour, Australia) correlates well with the PAC cardiac output (Wong et al, 2008; Su et al, 2008). Other USCOM measurements, such as Doppler estimation of peripheral artery pressures and left ventricular contractility, remain to be validated.

TEE has been gaining more popularity in liver transplantation (Burtenshaw & Isaac, 2006). Data from 2002 estimated use of TEE in only 21% of high-volume centers in the United States (Schuman, 2003), but a more recent survey showed that 86% of anesthesiologists in 40 large-volume U.S. centers use TEE in some or all liver transplantations (Wax et al, 2008).

The main advantages of TEE are that it provides continuous, real-time visualization of cardiac structures and dynamic function. TEE is a superior modality for estimating ventricular volume status, global LV contractility and ejection fraction, right ventricular function, segmental wall motion abnormalities, and septal motion. Doppler modalities allow for interrogation of transvalvular flows, dynamic left ventricular outflow obstruction, intracardiac shunts, and diastolic function. In addition, TEE is the only intraoperative monitor that allows an instantaneous diagnosis of pulmonary or intracardiac thrombus (Ellenberger et al, 2006; Planinsic et al, 2004) and pericardial or pleural effusion. TEE detection of a transpulmonary shunt as a positive bubble test in a patient with HPS is presented in Figure 97B.1.

Dynamic monitoring of the right ventricular function and detection of right ventricular failure are critically important in managing patients with portopulmonary hypertension, particularly during reperfusion. Assessment of right ventricular volume and contractility, severity of tricuspid regurgitation, and measurement of lows in the inferior vena cava (IVC) may help guide volume, inotrope, and pulmonary vasodilator therapy.

In addition to requiring significant training and resources, TEE has several important disadvantages. An obvious concern in the liver transplant patient population is the risk of rupture of gastroesophageal varices. Although this complication is very rare, it does emphasize the need for careful risk/benefit assessment of this monitoring modality in each individual recipient. It is prudent to withdraw the TEE probe from the stomach during surgical gastric retraction, making transgastric views inaccessible during most of the procedure. Another disadvantage is that TEE is not adept at providing and trending traditional numerical data (e.g., cardiac output), which are readily provided by the PAC. Visual assessments used in TEE are also highly operator dependent. Finally, unlike the PAC, the TEE probe is typically removed at the end of surgery; therefore the continuity of monitoring is interrupted, and the transfer of specific parameters of hemodynamic management to the postoperative ICU is difficult. This problem may be mitigated by the introduction of less expensive, disposable TEE probes.

Monitoring of Hemostasis

Conventional tests of hemostasis, PT and aPTT, have several important limitations (Dalmau et al, 2009; Ng et al, 2009). First, these assays utilize plasma samples devoid of platelets. The activated platelet surface, the naturally occurring medium of the in vivo coagulation, is replaced by addition of phospholipids. The contribution of platelets is thus not considered by these tests. Second, PT and PTT measure only the activity of procoagulant factors and do not take into account the anticoagulant factors. When PT is modified to include anticoagulant factors, thrombin generation in cirrhotic patients is not different from normal controls (Tripodi et al, 2005). The reported higher intralaboratory variability of INR than of PT may be of more relevance for MELD score determination than for acute intraoperative management (Lisman & Leebeek, 2007).

An important shortcoming of the conventional PT and PTT is a long turnaround time, typically about 45 minutes—suboptimal for an ongoing transplant surgery. Point-of-care (POC) assays require only a minimal delay between blood sampling and attaining the results of the test. POC assays of PT and PPT are quick (5 to 15 minutes), cartridge-type, whole-blood tests offered by several manufacturers. An acceptable agreement of such assays with corresponding plasma-based tests has been reported in OLT (Herbstreit et al, 2010), suggesting that the POC tests can effectively replace the slower, conventional testing.

Activated clotting time (ACT) was developed for POC monitoring of high-dose unfractionated heparin therapy, and it should be a part of the POC battery; with reperfusion of the graft, a massive dose of unfractionated heparin is flushed into the circulation. In conjunction with other POC tests, ACT may help guide the use and dosing of protamine.

TEG and ROTEM are POC assays that measure viscoelastic properties of whole-blood clot formation and lysis. Both technologies have been used to drive transfusion algorithms (Kang et al, 1985; Coakley et al, 2006). TEG measures time to onset of clot, rate of clot formation, clot tensile strength, and rate of clot lysis (Fig. 97B.2). Treatment of samples with an intrinsic pathway activator, kaolin, shortens clot formation, whereas addition of heparinase dissects the effects of exogenous heparin from intrinsic heparinoids. TEG results are available more rapidly than the conventional laboratory tests. In our institution, progress of TEG clot formation and lysis is displayed on a dedicated operating room monitor and is available to the anesthesiologist in real time.

FIGURE 97B.2 Intraoperative thromboelastogram (TEG) recordings from three orthotopic liver transplantation patients with different hemostatic derangements. In each panel, a “normal” TEG trace, generated by the instrument, is presented with an interrupted line. A, Hypercoagulable state in a patient with primary biliary cirrhosis. B,

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