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CHAPTER <strong>108</strong> ■ Liver Transplantation: Anesthetic Considerations 1817 by technetium 99 radio-labeled microalbumin scan or contrastenhanced echocardiography. Although 95% of the microaggre - gated albumin is taken up in the lungs of a normal individual, intrapulmonary shunting in HPS causes the radio-labeled micro - albumin spheres to be taken up in the systemic capillary beds. 1,19 Agitated saline contrast echocardiography can give a quick diagnosis if bubbles appear in the left atrium in the absence of a direct intracardiac communication. 13 Gastrointestinal System Portal hypertension and chronic malnutrition may predispose patients to spontaneous bacterial peritonitis and other infections due to impaired immune function. Children who have undergone Kasai portoenterostomy may also be at increased risk for devel - oping cholangitits. Hypersplenism and associated thrombocy - topenia resulting from portal hypertension can lead to catastrophic hemorrhage, especially in the presence of esophagogastric varices and coagulopathy. 7 Aspiration of blood during an acute variceal bleed may cause pulmonary decompensation. Hepatic System Impaired hepatic synthetic function may affect drug metabolism, glucose homeostasis, intravascular volume, and coagulation. De - creased glycogen stores and impaired gluconeogenesis may pre - dispose to hypoglycemia if supplemental glucose is not provided. Coagulation defects result from reduced hepatic synthesis of clotting factors as well as malabsorption of vitamin K secondary to decreased bile acid secretion and antibiotic therapy. A deficiency of vitamin K–dependent clotting factors may lead to severe bleeding. Portal hypertension results in the development of gastrointestinal varices as well as ascites. Anemia and thrombocytopenia which are commonplace in end stage liver disease, are exacerbated by dilutional effects from increased plasma volume. 7 Anemia may result from bleeding, malnutrition, and splenic sequestration of red blood cells. Thrombocytopenia is commonly secondary to splenic sequestration, but it may also occur as a result of sepsis. 7 Impaired metabolism of drugs, including anesthetic agents, may result in prolongation of their duration of action. Impaired protein synthesis, in addition to increased blood volume and volume of distribution, results in decreased plasma concentrations of coagulation proteins, plasma cholinesterase, and albumin. High serum levels and prolonged elimination half-lives of anesthetic drugs that are highly protein-bound and have small volumes of distribution, can occur. However, drug protein binding does not correlate well with albumin concentrations or the degree of liver dysfunction. 20 Serum albumin concentrations are also influenced by malnutrition and degradation. Because albumin has a half-life of approximately 21 days, serum levels may not reflect current albumin production. 7 Hypoalbuminemia results in low serum oncotic pressure which leads to intravascular hypovolemia and hypotension, interstitial edema, ascites, and pleural effusions. 7,21 Renal System The majority of children presenting for liver transplantation have adequate renal function. Hepatorenal syndrome is characterized by decreased renal blood flow, glomerular filtration rate and urine output, as well as elevated serum creatinine, low urine sodium (
1818 PART 5 ■ Anesthetic, Surgical, and Interventional Procedures: Considerations arterial and venous catheters, particularly in the presence of coagulopathy. Pulmonary artery catheters may provide useful hemodynamic information, but are not usually employed in pediatric liver trans - plantation due to potential complications and size incom patibility. Transesophageal echocardiography (TEE) can provide real time monitoring of ventricular filling and contractile function, which may help with fluid and inotropic drug management. 7 TEE can also help to detect septal defects or a patent foramen ovale which can predispose to paradoxical air emboli, as well as detect intra - cardiac air or microthrombi during hepatic reperfusion. Anesthesia is maintained with a balance of inhalational agent, opioid, and nondepolarizing muscle relaxant. Isoflurane does not undergo significant metabolism and it has not been associated with renal or hepatic toxicity. 7 Midazolam may be useful in pro - viding hypnosis and amnesia when use of inhalational anesthetic agents is limited by hypotension. Administering an FiO 2 of 1.0 during hypotensive episodes may maximize oxygen delivery to tissues. Liver transplantation surgery is divided into three phases. The preanhepatic or dissection phase begins with skin incision and terminates with occlusion of the hepatic artery and portal vein. This is followed by the anhepatic phase which begins with devascularization of the liver or hepatectomy and is completed when the I.V. and portal vein clamps are removed and the newly transplanted liver is perfused, with or without unclamping of the hepatic artery. The final phase, the postanhepatic or postreperfusion phase, begins immediately after the new liver graft is reperfused and ends with completion of surgery. Each phase presents specific anesthetic challenges and management goals. Dissection (Preanhepatic) Phase In this first phase of surgery, there is potential for significant blood loss during dissection of the diseased liver in the presence of coagulopathy. Patients who have had previous upper abdominal surgeries such as a Kasai procedure or previous liver trans planta - tion are more likely to experience significant blood loss associated with adhesions and prolonged dissection. 1,27 In fact, the greatest blood loss typically occurs during this stage and during the beginning of the anhepatic stage. Anesthetic management is aimed at maintaining hemodynamic stability and glucose homeostasis. Arterial blood gases should be assessed hourly. Fluid and blood product administration, and judicious correction of coagulation abnormalities can be guided by serial hematocrit measurements, prothrombin time, and throm - boelastography (TEG). Overcorrection of coagulopathy must be avoided. Fresh frozen plasma may be administered to achieve an INR near 1.5, and platelets may be administered to maintain platelet counts greater than 50,000/mm 3 or when there is evidence of thrombocytopenia by TEG. 1,7 However, it should be noted that the TEG has lengthy endpoints, such that the coagulation profile may have changed significantly by the time TEG results become available. It is therefore necessary to communicate with the surgeons and correlate test results with the clinical picture. Correction of coagulopathy should be directed by coagulation studies that differentiate particular clotting defects, and clinical correlation. Overly aggressive correction of coagulation abnor - malities may contribute to hepatic artery and/or portal vein thrombosis, especially during the reperfusion phase. If the pro - thrombin time (PT) and partial thromboplastin time (PTT) are markedly prolonged, and the surgeon observes diffuse bleeding, 10 mL/kg of fresh frozen plasma should be administered. Further transfusion therapy should be guided by close monitoring of coagulopathy. Fresh frozen plasma transfusions at rates exceed ing 1 mL/kg/min will depress the ionized calcium concentration, causing hypotension and, in extreme cases, electromechanical dissociation. Calcium levels should be monitored closely during massive blood loss necessitating rapid transfusion of blood products. Ionized calcium should be maintained at greater than 1 mmol/L. A calcium chloride infusion may be initiated to main - tain ionized calcium at a target level of 1.2 mmol/L. 1 The higher concentration of citrate in FFP significantly chelates elemental calcium and magnesium ions in blood. Citrate intoxication is the most common complication of massive transfusion of blood products, especially during the anhepatic phase when citrate cannot be metabolized. Thrombocytopenia may be secondary to preoperative hyper - splenism, platelet consumption, or intraoperative dilution. Platelet therapy is reserved for treating platelet counts less than 50,000 mm 3 in the presence of excessive surgical bleeding. Fibrinogen depletion as a result of fulminant hepatic failure leads to pro - longation of both PT and PTT. Excessive surgical bleeding with associated fibrinogen depletion should be corrected with cryoprecipitate 0.2 units/kg. The treatment of coagulopathy, especially with cryoprecipitate and platelets, should be discussed with the surgeon, who will be able to assess coagulation abnormalities in the surgical field. Ideally, the hematocrit should be maintained in the range of 26% to 30% to minimize risk of thrombotic complications asso - ciated with increased viscosity. 1,28 Massive transfusion of banked red blood cells to infants can result in severe hyperkalemia. Irra - diation of blood products is not necessary in liver trans plantation as graft versus host disease in liver recipients is almost always due to the donor organ. 29,30 Irradiated blood should not be used routi - nely for infants undergoing liver transplantation because irradia - tion of packed red blood cells can increase the potassium concentration in the supernatant by two- to threefold. Nonirra - diated blood that is as fresh as possible should be requested from the blood bank when infants are undergoing liver trans - plantation as massive transfusions of blood greater than 2 weeks of age has been associated with severe intraoperative hyperkalemia and cardiac arrest in infants. 31,32 Massive blood transfusions are also associated with dilutional coagulopathies, acidosis, and hypo - thermia. Fluid administration and occasionally inotropic support may be necessary to treat hypotension. Systemic vascular resistance (SVR) is often unresponsive to -agonists in liver failure patients, and may exacerbate peripheral and renal ischemia in high con - centrations. Surgical manipulation of the liver may also contribute to hypotension by impeding venous return. Sodium bicarbonate should be administered to maintain a base deficit above negative 6 mEq/L. Intravenous dextrose (D5 NS) should be administered to maintain serum glucose concentration greater than 100 mg/dL. These patients are prone to hypoglycemia due to impaired glu - coneogenesis and glycogen storage. Impaired hepatic degradation of insulin may further exacerbate hypoglycemia. There is no consensus on the optimal replacement fluid, which tends to vary with institutional preference. Additional fluid replacement is most often given as balanced salt and/or colloid solution. Albumin solution may be used for intravascular
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Chapter 108

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