Anesthesia for Hepatic Surgery

Hepatic Surgery

Common hepatic procedures include repair of lac-erations, drainage of abscesses, and resection of primary or metastatic neoplasms, and up to 80% to 85% of the liver can be resected in many patients. In addition, liver transplantation is performed in many centers. The perioperative care of patients undergoing hepatic surgery is often challenging because of coexisting medical problems and debili-tation found in many patients with intrinsic liver disease, and because of the potential for signifi-cant operative blood loss. Hepatitis and cirrhosis greatly complicate anesthetic management and increase perioperative mortality. Multiple large-bore intravenous catheters and fluid blood warm-ers are necessary; rapid infusion devices facilitate management when massive blood transfusion is anticipated. Continuous intraarterial pressure monitoring is typically utilized.

Hemodynamic optimization is often compli-cated by the conflict between the need to maintain sufficient intravascular volume to ensure adequate hepatic perfusion and the need to keep central venous pressure low to minimize liver engorgement and surgical bleeding.” Central venous pressure measurement is not an accurate monitor of volume status, and, when this determination is important, the appropriate alternative modality is goal-directed therapy utilizing esophageal Doppler, arterial wave-form analysis, or TEE. Care should be taken in plac-ing an esophageal Doppler or TEE probe in a patient with esophageal variceal disease.

Some clinicians avoid hypotensive anesthesia because of its potentially deleterious effects on liver tissue, whereas others believe that it can reduce blood loss when used judiciously. Administration of antifibrinolytics, such as ε-aminocaproic acid or tranexamic acid, may reduce operative blood loss. Hypoglycemia, coagulopathy, and sepsis may occur following large liver resections. Drainage of an abscess or cyst may be complicated by perito-neal contamination. In the case of a hydatid cyst, spillage can cause anaphylaxis due to the release of Echinococcus antigens.

Postoperative complications include hepatic dysfunction, sepsis, and blood loss secondary to coagulopathy or surgical bleeding. Severe postoper-ative pain from the often extensive surgical incision may hinder postoperative mobilization and conva-lescence, but perioperative coagulopathy may limit the use of epidural analgesia. Infusion of local anes-thetic into the surgical wound can reduce the need for opioids. Postoperative mechanical ventilation may be necessary in patients undergoing extensive resections.

Liver Transplantation

When a center opens a liver transplantation pro-gram, a credentialed director should be appointed to the anesthesia component. This individual should be an anesthesiologist with experience and training in liver transplantation anesthesia. A dedicated team of anesthesiologists should be assembled to manage the perioperative course of all liver transplantation patients. This team should have a thorough under-standing of the indications for, and contraindications to, liver transplantation ( Tables 33–9 and 33–10), as well as associated comorbidities (eg, coronary artery disease, cirrhotic cardiomyopathy, portopulmonary hypertension, hepatopulmonary syndrome, hepa-torenal syndrome and hepatic encephalopathy and cerebral edema). It has been demonstrated that such an approach improves outcomes, as measured by

reduced blood transfusions, the need for postopera-tive mechanical ventilation, and the duration of stay in the intensive care unit.

Preoperative Considerations

The Model for End-stage Liver Disease (MELD) score is used by the United Network for Organ Sharing (UNOS) to prioritize patients on the wait-ing list for a liver transplant. The score is based on the patient’s serum bilirubin, serum creatinine, and INR, and is a predictor of survival time if the patient does not get a liver transplant. A score of 20 pre-dicts a 19.6% risk of mortality at 3 months, whereas a score of 40 predicts a 71.3% risk of mortality atmonths (Figure 33–1).

The MELD score

= 0.957 × log_e[serum creatinine (mg/dL)] + 0.378 × log_e[total serum bilirubin (mg/dL)] + 1.120 × log_e[INR]

Multiply the resulting value by 10, and round to nearest whole number. The minimum for all values is 1.0; the maximum value for creatinine is 4.0.

Most liver transplant candidates have high MELD scores and present with jaundice, renal fail-ure, and coagulopathy. They may also be emaci-ated and have massive ascites, and some may have encephalopathy, hepatopulmonary syndrome, cir-rhotic cardiomyopathy, and POPH. The typical hemodynamic finding is a high cardiac index and low systemic vascular resistance.

Significant blood loss may be anticipated, and large-bore intravenous catheters should be placed for access. A rapid infusion pump should be avail-able. Routine hemodynamic monitoring should include intraarterial pressure monitoring and a central venous catheter. TEE is routinely utilized

in many centers. Pulmonary artery catheterization, once routine, has now been abandoned for liver transplant patients at many centers.

The immediate availability of intraoperative continuous venovenous hemodialysis (CVVHD) may be very helpful for volume management in the patient with marginal or no renal function. In patients with significant electrolyte abnormalities, serum sodium and potassium can be closely man-aged by adjusting the CVVHD dialysate solution.

Intraoperative Management

As noted above, hepatic disease causes endothelial dysfunction that impairs all organs of the body. The heart develops cirrhotic cardiomyopathy; the brain, encephalopathy and eventual cerebral edema; the kidneys, hepatorenal syndrome and eventual acute tubular necrosis; and the lungs, hepatopulmonary syndrome and/or portopulmonary hypertension. Therefore, each organ must be carefully managed throughout the operative procedure and the postop-erative period.

Maintenance of cerebral perfusion pressure is particularly important in patients with cerebral edema, and many centers will temporarily correct the coagulopathy in order to place an intracranial transducer for monitoring intracranial pressure. Additional cerebral protective measures include head elevation of 20°, mild hypothermia, and mild hypocarbia with vasopressor support to maintain mean arterial pressure. When the patient’s head is elevated, the arterial pressure transducer should be zeroed at the level of the external auditory meatus for accurate determination of cerebral perfusion pressure.

The coagulopathy is managed with the aid of a point-of-care viscoelastic coagulation assay device (TEG ®, ROTEM®, or Sonoclot®) or frequent assessment of conventional tests of coagulation. Blood loss may be significant, and transfusions are targeted to maintain the hemoglobin level >7 g/dL.

Transfusions must be tempered to keep the central venous pressure (CVP) low during the liver dissection to reduce blood loss and minimize liver congestion, and at reperfusion and during the remainder of the procedure to prevent graft conges-tion and hepatic dysfunction. Most coagulopathies will correct with the new liver if its function is good. Fibrinolysis, a low ionized calcium level, and hypo-thermia must be corrected, as these may promote bleeding. However, coagulation defects usually do not need to be treated preoperatively or intraopera-tively unless bleeding is a problem. Intraoperative transfusion of platelets and fresh frozen plasma is associated with decreased long-term patient survival.

The liver transplantation surgical procedure is divided into three stages: dissection (preanhepatic), anhepatic, and neohepatic periods.

The dissection (preanhepatic) phase is high-lighted by the management of hemodynamic changes related to blood loss and surgical com-pression of major vessels. Hyponatremia should be carefully managed without rapid serum sodium cor-rection, because this may promote the development of central pontine myelinolysis. Hyperkalemia may require aggressive intervention with diuresis, trans-fusion of only washed packed red blood cells, or CVVHD. Citrate toxicity (hypocalcemia) will occur rapidly if blood is transfused; therefore, ionized calcium should be closely monitored, and calcium chloride administered as necessary. A low CVP is helpful to minimize blood loss while systemic arte-rial pressure is maintained.

The anhepatic phase begins with the vascu-lar occlusion of the inflow to the liver and ends with reperfusion. Some centers utilize venovenous bypass to prevent congestion of the visceral organs and improve venous return. It may protect kidney function.

In the neohepatic phase, two pathophysiologi-cal events may occur on opening the portal vein and allowing reperfusion of the graft. The first is a reperfusion syndrome caused by the cold, acidotic, hyperkalemic solution that may contain emboli and vasoactive substances being flushed from the graft directly into the right heart. This may cause hypotension, right heart dysfunction, arrhythmias, and even cardiac arrest, and may be preempted to some extent by the prophylactic administra-tion of calcium chloride and sodium bicarbonate. The second syndrome that may occur is ischemia/ reperfusion injury. This may result from impaired reperfusion due to severe endothelial dysfunction,and, in rare cases, may lead to primary nonfunc-tion of the graft.

Postoperative Management

Patients who undergo liver transplantation are often severely debilitated and malnourished and have multiorgan dysfunction; therefore, they will need careful support until they have recovered. Continuous monitoring of cardiovascular, pulmo-nary, renal, and neurological status is necessary. Early extubation is appropriate in selected patients if they are comfortable, cooperative, and not exces-sively coagulopathic. Immunosuppression must be precisely managed to minimize the risk of sepsis. A close watch on graft function must be maintained, with a low threshold for checking hepatic artery patency and flow. Postoperative bleeding, biliary leaks, and vascular thromboses may require surgi-cal reexploration.