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Recent Developments in
Transplantation Medicine

Liver Transplantation

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Anesthesia Considerations in Liver Transplantation

Michael A.E. Ramsay

Contents

Tables and Figures

  • Table 1. Electrolyte changes with cell-saver processing

Introduction

Liver transplantation is now a routine procedure performed in numerous medical centers throughout the world. Currently, about 250 liver transplants are performed in the United States every month. The introduction of the University of Wisconsin preservation solution has allowed ischemic times in excess of 12 hours without detriment in outcome, permitting the recipient procedure to be done on a semi-elective basis at a reasonable time of day, reducing the fatigue factor on members of the team. This plus numerous other advances has shortened the procedure time to under six hours and minimized utilization of blood products.

The main indications for orthotopic liver transplantation (OLTX) in adults are alcoholic cirrhosis, chronic cirrhosis due to non-A, non-B hepatitis and hepatitis C, primary biliary cirrhosis, cryptogenic cirrhosis, and primary sclerosing cholangitis. Only a minority of recipients are transplanted for cirrhosis due to hepatitis B, fulminant hepatic failure, malignancy, autoimmune cirrhosis, and a variety of inborn errors of metabolism.1 The most common indication for OLTX in pediatric patients is biliary atresia, followed by metabolic disorders, fulminant hepatic failure, cryptogenic cirrhosis, neonatal hepatitis, and malignancy.

Lack of suitable donors is the major factor limiting this operation and has resulted in the deterioration of functional status in recipients. In 1991 in the U.S. over half (51%) of all liver transplant recipients were in intensive care units, and 29.5% were on life support. This means that many recipients undergo OLTX with multiorgan system dysfunction, making perioperative complications more likely.

According to UNOS (United Network for Organ Sharing) data for OLTX performed between October 1, 1981 and December 31, 1991, the major cause of death following the procedure was infection, followed by cardiovascular complications, hemorrhage, malignancies, primary hepatic nonfunction, multiorgan failure, recurrent disease, operative death, and rejection. Most deaths occurred within the first week following OLTX, and the most common causes of death during that interval were cardiovascular disease (28.2%), operative mortality (14.6%), primary graft failure (13.5%), and hemorrhage (13.0%). Between weeks 2 and 4, over half the deaths resulted from infectious complications. The challenge facing all members of the transplant team, including the anesthesiologist, is to reduce the morbidity and mortality of this procedure.

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Anesthetic Donor Management

Anesthesia care includes the intensive management of the organ donor. It is imperative to optimize the care of the donor to allow retrieval and successful transplantation of even marginal organs. Major hemodynamic variability and instability are very commonly seen in donors, especially during the harvest when all major organs may be removed.2,3

The intensive management of the donor is critical to the harvesting of potentially viable grafts. It is prudent to utilize all the monitoring sensors and laboratory facilities that would be used on living patients, so that organ perfusion may be maintained and, if necessary, improved. Invasive monitoring is thoroughly justified so that hemodynamic parameters can be calculated and manipulated to ensure adequate cardiac output and tissue perfusion. An elevated blood pressure alone does not indicate that there is adequate blood flow through major organs. Inotropic agents should be titrated carefully, using the full range of drugs available, to improve hemodynamics. In this way "cookbook" regimens that include maximum doses of inotropes, and minimum blood pressures that must be maintained are avoided. This allows the potential donor pool to be enlarged, and enhances organ preservation.

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Preoperative Patient Evaluation

The disease process and the transplant operation cause major physiological changes. All transplant team members must participate in the selection and preoperative assessment of the recipient so that potential responses to intraoperative stresses can be anticipated and unsuitable candidates rejected. The ramifications of liver disease may affect all major organ systems, creating a major challenge for the anesthesiologist. These patients are often cachectic, with hepatic failure, multiorgan dysfunction, encephalopathy, and severe metabolic derangements. Contraindications to transplantation include acquired immune deficiency syndrome, major sepsis, metastatic malignancy, untreated alcoholism, severe pulmonary hypertension, and severe cardiac disease.

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Cardiovascular System

The cardiovascular system is difficult to evaluate in patients with severe liver disease. The typical high cardiac output state with low systemic vascular resistance seen in most patients with cirrhosis can masquerade as an athletic heart, disguising severe cardiomyopathy. The reduced afterload often obscures this dysfunction, leading to a false sense of confidence in the cardiac performance of the recipient. Patients with alcoholic cirrhosis in particular may lack the cardiac reserve their hyperdynamic circulation suggests. Experience in the cardiologic assessment of this patient group is necessary for accurate interpretation of ventricular function on echocardiography. In patients suspected of having ventricular dysfunction, functional cardiac reserve should be assessed by exercise radionuclide scintigraphy, which will help detect not only cardiomyopathy but also coronary artery disease and severe pulmonary hypertension as well. Endomyocardial biopsy may be necessary for complete evaluation of suspected cardiomyopathy.

Severe coronary artery disease is found in less than 3% of this patient population. It is thought that cirrhosis may offer some protection from coronary atherosclerosis.4 Coronary artery disease need not represent a contraindication to liver transplantation. Many stenotic lesions may be amenable to percutaneous transluminal coronary angioplasty (PTCA). In those few patients in whom PTCA is not possible, cardiologists and the transplant team must decide whether to perform coronary revascularization or liver transplantation first, or whether the patient is a suitable candidate for OLTX at all.

Cardiac surgery in the patient with severe liver dysfunction is hazardous because of the pre-existing coagulopathy and the potential for fulminant hepatic failure. If OLTX is performed first, the hemodynamic changes that can occur during and after the procedure may precipitate an acute myocardial infarction. Morris et al recommend that coronary revascularization should precede OLTX.5

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Pulmonary Function

Intrapulmonary and extrapulmonary shunts may develop in the lung in association with portal hypertension. The resultant right-to-left shunt can cause severe hypoxia and a risk of systemic air embolism during transplantation.

Severe pulmonary hypertension sometimes occurs with portal hypertension.6 The pulmonary hypertension may progress rapidly and, if irreversible, causes a high intraoperative mortality.7 Nitric oxide is an ideal investigational agent to test the reversibility of pulmonary hypertension because of its rapid action, potent pulmonary vasodilatation, and lack of systemic effect. Pulmonary hypertension is often first detected in the operating room just prior to anesthesia and transplantation when the pulmonary artery catheter is placed. A prompt attempt to reverse the hypertension with a pulmonary vasodilator such as prostaglandin E1 (PGE1) should be made. PGE1 infusion is titrated up from 0.02 mg/kg/min until the desired effect is obtained or until systemic hypotension limits its use. If severe pulmonary hypertension persists, with mean pressures greater than 40 mm Hg and pulmonary vascular resistance greater than 350 dyneslseclcm-5, then another recipient should be considered for the donor organ because of the very high mortality rate under these circumstances.8

Adult respiratory distress syndrome (ARDS) is a sinister complication of end-stage liver disease; the syndrome is fatal unless transplantation is performed.9 Sepsis as the etiology of ARDS must be ruled out by bronchoalveolar lavage and brush specimen cultures from diseased lung segments. The intraoperative management of such a patient with ARDS undergoing OLTX may require a more sophisticated ventilator than usually available in the operating room. The Siemens 900 series (Siemens-Elema AB, Solna, Sweden), which allows continuous assessment of peak airway pressures, expired tidal volumes, and positive end-expired pressures, is well designed for these patients.

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Coagulation Disorders

Patients with liver disease often have major coagulation abnormalities, with bleeding a common complication. The frequent coexistence of bleeding varices, nutritional deficiencies, coagulopathy, and splenomegaly often produces anemia and thrombocytopenia as well. The coagulopathy stems from reduced synthesis of most coagulation factors (I, II, V, VII, IX, and X), decreased synthesis of plasminogen activator inhibitor, and decreased hepatic clearance of plasminogen activator causing fibrinolysis.10 Platelet dysfunction may also be present in those patients with concomitant renal dysfunction. The prothrombin time is the best indicator of decreased hepatic synthesis of coagulation factors.

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Renal Function

Renal function may be impaired in patients with liver failure. This can be due to the same disease process that damaged the liver, or the result of prerenal azotemia, acute tubular necrosis, or hepatorenal syndrome. In end-stage liver disease, the renin-angiotensin system is activated with little or no sodium excretion. Also, antidiuretic hormone activity is increased, causing water retention that exceeds sodium retention, resulting in hyponatremia. Hepatorenal syndrome is characterized by normal urinary sediment, low urinary sodium, azotemia, and oliguria. This picture is similar to prerenal azotemia; it is therefore important to exclude hypovolemia. Patients with hepatorenal syndrome usually recover renal function following OLTX.11 If a renal biopsy demonstrates irreversible renal disease, then a combined liver and kidney transplant should be considered.

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Portal Hypertension

Portal hypertension may develop as a result of hepatic cirrhosis. The complications of portal hypertension include variceal hemorrhage, ascites, and portosystemic encephalopathy. Two hypotheses of the pathophysiology of portal hypertension have been put forward. The backward flow theory proposes that the shrunken cirrhotic liver affords a significant resistance to portal flow. The forward flow theory emphasizes the hyperdynamic splanchnic flow. Portal hypertension is commonly defined as a wedged hepatic venous pressure gradient of 10 mm Hg or higher. Hepatic vein pressure gradients greater than 16 mm Hg are associated with an increased incidence of bleeding and death.12

The reduction of portal hypertension is essential if these patients are to survive to transplantation. Treatment may be pharmacological, endoscopic, surgical, angiographic, or a combination. Of these, beta-blockers decrease cardiac output and splanchnic hyperemia; the dose is titrated to reduce the resting heart rate by 25%. Vasoconstrictors such as vasopressin administered in a dose of 0.4 to 0.8 units per minute by continuous infusion are also very effective. Varices may be ligated or sclerosed endoscopically.

If these methods fail to stop variceal bleeding, surgical creation of portosystemic shunts, such as the distal splenorenal shunt, may be lifesaving. Portal decompression can also be performed in the radiology department, using the transjugular intrahepatic portosystemic shunt (TIPS) procedure. The internal jugular vein is catheterized, giving access to the hepatic vein, and a stent is placed across a fistula created between the hepatic vein and the portal vein.13 This procedure may be performed under conscious sedation, but in our experience general anesthesia is preferable, allowing better control of oxygenation and ventilation and minimizing patient discomfort. The availability of intensive monitoring and immediate access to laboratory and blood bank services are essential; these procedures can develop into major management exercises performed in an area remote from the operating room.

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Fulminant Hepatic Failure

Patients may present for transplantation in fulminant hepatic failure with a severe coagulopathy, encephalopathy, metabolic derangements, and often renal failure. Loss of hepatic gluconeogenesis causes lactic acidosis from anaerobic metabolism and hyperglycemia. Serum ammonia levels increase as the liver is unable to convert ammonia to urea. The prolongation of the prothrombin time is a sensitive index of hepatocyte dysfunction. If a donor liver is not immediately available and the patient's demise is imminent, then a total hepatectomy may be performed, together with a portocaval shunt, as a lifesaving measure. Patients improve following hepatectomy, with less metabolic acidosis and less need for vasoactive support; successful transplantation can proceed up to 37 hours later.14,15

Encephalopathy may present a varied clinical picture, ranging from mild confusion to deep coma with cerebral edema. In the early stages of encephalopathy, benzodiazepine drugs should be avoided because these agents increase g-aminobutyric acid neurotransmissions which exacerbate mental stupor.16 Early control of the airway is essential to protect the brain from increasing edema. If significant edema occurs, intracranial pressure is best monitored by the placement of an intracranial pressure sensor to allow optimal protective measures.17

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Anesthetic Management

Pharmacodynamics and Pharmacokinetics

Varied responses to drug administration must be expected in patients with liver disease; therefore, careful monitoring of drug actions is necessary, with titration of drug to effect. Hypoalbuminemia develops almost universally with chronic liver disease, resulting in fewer drug binding sites and an increase in free drug at the site of action. Metabolism and clearance depend on the state of liver blood flow and the integrity of the P450 cytochrome system in hepatocytes. Biotransformation by conjugation is often better preserved, so that drugs like morphine and propofol that rely on this pathway may be better tolerated.18 Coexisting renal failure may also prolong the action of drugs that rely on renal excretion for clearance. Because of salt and water retention, the volume of distribution is increased, requiring larger initial doses of some drugs. Different disease states present with different patterns of liver dysfunction. Careful monitoring of drug action and titration of dose to achieve the desired clinical effect is required.

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Preoperative Management

Preoperative management commences with the multidisciplinary patient selection conference where patients are evaluated in depth and any anesthetic concerns are raised. The patient is placed on a waiting list; 6-8 months may elapse before an organ becomes available. Deterioration in the patient's physical condition often occurs during this time; therefore, the anesthesiologist must reexamine the patient and reevaluate the clinical picture on admission for transplantation. Fortunately, the use of the University of Wisconsin (UW) solution as a preservative has led to the performance of liver transplantation on a semi-elective basis rather than as an emergency. This allows time for a proper preoperative assessment and the opportunity to obtain further laboratory data. Preoperative medications should include "full stomach" prophylaxis with ranitidine, metoclopramide, and particulate-free antacid. Benzodiazepines should be avoided in preencephalopathic patients, and intramuscular injections should be avoided in patients with coagulopathies.

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Monitoring

Liver transplantation requires the management of severe coagulopathy, metabolic derangements, massive fluid shifts, blood loss, temperature derangement, hemodynamic instability, and renal dysfunction. Full invasive monitoring is mandatory, with direct arterial, central venous, and pulmonary artery pressure sensors so that hemodynamic profiles can be calculated and appropriately managed. The presence of a "stat lab" in the immediate operating suite area allows rapid analysis of hemostasis profiles, electrolytes, glucose, and blood gases. The presence in the operating room of a Thrombelastograph® (Haemoscope Corp., Morton Grove, IL) allows "on-line" assessment of the quality of clot formation.

Adequate venous access is necessary to permit rapid massive transfusions if required. Fluid warming devices should be in-line, and additional temperature maintenance is provided by a heated humidifier, warming blanket, and a forced-air warming device. In the (rare) event that large volumes of warmed blood are needed at high flow rates, a rapid infusion device should be available (Rapid Infusion System, Haemonetics Corporation, Braintree, MA). Caution is necessary when rapidly transfusing older units of packed red cells because the high potassium content may cause a sudden rise in serum potassium to dangerous levels in the patient.

The use of a cell-saver helps reduce the demand on the blood bank for red cells. The cell-saver may be used in all cases except those with malignant tumors. Patients in hepatorenal failure with elevated blood levels of ammonia, lactate, and potassium may be auto-exchange-transfused with the cell-saver, taking off the unwanted electrolytes, citrate, and excess volume and returning red cells. This strategy may create intravascular space for transfusions of blood products such as fresh-frozen plasma, cryoprecipitate, and platelets to improve coagulation (Table 1).19

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Anesthetic Technique

Because of the possiblity of delayed gastric emptying, a routine rapid sequence induction should be performed. Induction with pentothal or ketamine with succinylcholine or vecuronium are techniques that work well. Maintenance of anesthesia with isoflurane in an air-oxygen mixture supplemented with sufentanil and vecuronium provides optimal conditions. Vecuronium is used so that the function of the new liver graft may be evaluated. The time for the return of a train-of-four (TOF) mode with a nerve stimulator correlates well with the function of the new graft.20 A primary nonfunctioning graft or a dysfunctioning graft can be detected early by a delayed return of TOF, and either the patient listed on the computer for a retransplant or PGE1 started as an infusion in an effort to resuscitate the graft.

Table 1.Electrolyte changes with cell-saver processing

Positioning and padding of the patient requires particular care because the procedure may take many hours. The incidence of postoperative neuropathies is significant.21

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Intraoperative Management

The operation is considered in three phases. The preanhepatic phase is when the liver is mobilized, the anhepatic phase when the liver is removed, often accompanied by veno-venous bypass, and the third or neohepatic phase is when the new liver graft is reperfused and the operation completed. Each phase requires careful consideration by the anesthesiologist.

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Preanhepatic Phase

During this period a further evaluation of coagulation status should be made both qualitatively, using the Thrombelastograph and observing the surgical field, and quantitatively, by sending a blood sample to the "stat-lab" for a hemostasis profile. Major fluid shifts may occur as liters of ascitic fluid are drained and large varices transected. Hypotension may result from surgical manipulation of the liver, temporarily obstructing venous return. Aggressive correction of a coagulopathy is not usually necessary at this stage unless bleeding is excessive. Routine cross-match orders for five units of packed red cells and five units of fresh frozen plasma should be a sufficient reserve at this time.

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Anhepatic Phase

Total hepatectomy is performed with transection of the portal vein, the hepatic artery, and the inferior vena cava above and below the liver. Significant changes in hemodynamic indices may follow: decreased venous return causing a fall in cardiac output, increased splanchnic and lower caval pressures, decreased renal perfusion pressure, and reduced systemic arterial pressure. Venovenous bypass is used routinely in some centers to facilitate venous return from the portal system and lower body to the heart via a centifugal pump to the axillary vein. The potential benefits of this bypass are maintained renal perfusion and reduction in vascular congestion of the intestines with less bleeding.22 The disadvantages are increased hypothermia and the risk of air and thromboembolism. Selective utilization of venovenous bypass has been recommended after a five-minute trial period of clamping the supra- and infrahepatic cava and portal vein. If mean systemic arterial blood pressure decreases by >30% or cardiac index decreases by >50% or both, then bypass is recommended.23

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Neohepatic Phase

This phase of the surgery is marked by the release of portal blood flow through the graft. Severe hemodynamic instability known as the postreperfusion syndrome may follow within a few minutes with severe hypotension, decreased heart rate, and a major decrease in systemic vascular resistance together with an increase in pulmonary artery pressure. The etiology appears to be the sudden influx of a cold, acidic, hyperkalemic fluid into the circulation. Other mediators may also be released by the ischemic liver including xanthine oxidase, a generator of cytotoxic oxygen radicals which may produce myocardial dysfunction and cellular damage. The treatment of the syndrome may require strong vasopressors with an alpha-agonist action such as norepinephrine.24

Following reperfusion of the graft and stabilization of the hemodynamics, the liver should appear pink and well perfused. Some livers may appear marginal at this time; they may be improved by the infusion of PGE1. PGE1 has a beneficial effect on vascular endothelium that enhances blood flow through the graft both generally and in areas of "no reflow," and may also be effective in reversing hepatocellular damage.25

Coagulopathies should be corrected during this stage of the procedure to obtain excellent hemostasis. Fibrinolysis, if detected by the Thrombelastograph, should be reversed with aminocaproic acid, and if heparin is detected (from the donor surgery), reversal with protamine is indicated.26

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Fluid and Metabolic Considerations

Maintenance with intravenous fluid that does not contain lactate is a prudent choice in a patient with poor liver function and possible lactic acidosis. Infusion of crystalloid is guided by renal function and hemodynamic parameters. Urine output is optimized first by a fluid challenge followed by osmotic diuretics and loop diuretics. A dopamine infusion may also be beneficial in promoting urine output.27 For anuric patients, intraoperative continuous arteriovenous hemofiltration can be a very effective means of removing unwanted volume. Citrate metabolism is impaired in patients with liver failure; therefore, ionized calcium levels should be monitored closely. Transfusion of citrated blood products may result in citrate toxicity. Hypocalcemia may require frequent bolus doses of calcium chloride 10mg/kg to prevent myocardial depression and hypotension. Blood transfusions and blood product administration are given in accordance with clinical need and information derived from Thrombelastograph and laboratory results. As the transplant team gains experience working together, transfusion of blood products may decrease, allowing many cases to proceed without the need to draw on blood bank reserves at all.

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Postoperative Management

If the new liver is functioning well, the patient can be extubated within two hours and transferred out of the intensive care unit within 24 hours. Marginal grafts may respond to continued infusions of PGE1 and careful management of fluid, electrolyte, and coagulation status.

Postoperative bleeding requires early surgical intervention so that large clots do not accumulate, promoting further coagulopathy or providing a nidus for infection. The rare development of adult respiratory distress syndrome (ARDS) is associated primarily with sepsis.28 Postoperative pain can be well controlled with the use of a patient-controlled analgesia (PCA) pump.

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Summary

Anesthesia considerations for liver transplantation include the management of severely deranged physiology, pharmacology, and biochemistry, as all organ systems may be affected adversely by the failing liver. A close working relationship between all members of the operating team is necessary for the success of the program. The development of such teams in major transplant centers has resulted in a marked reduction in the morbidity and mortality of this procedure and a concomitant reduction in the cost. The future will include developing further techniques that will enhance donor organ availability. Reduced size liver grafts from living related donors or from splitting harvested organs will be utilized with increased frequency. As improved immunosuppressive therapy becomes available, xenografts may become a clinical reality. Gene therapy trials are underway using viral vectors to alter the genetic makeup of hepatocytes in order to correct metabolic disorders. Artificial liver support systems will become a bridge to recovery or transplantation in patients with fulminant hepatic failure. All of these advances will have an impact on the anesthesiologist.

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References

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  2. Duke PK, Ramsay MAE, Paulsen AW, Gunning TC, Roberts LC, Swygert TH, et al. Intraoperative hemodynamic heterogeneity of brain dead organ donors. Transplant Proc 1992;53:383-386.
  3. Pickett JA, Wheeldon D, Oduro A. Multi-organ transplantations: donor management. Curr Op Anaesthesiol 1994;7:80-83.
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  5. Morris JJ, Hellman CL, Gawey BJ, Ramsay MAE, Valek TR, Gunning TC, et al. Two patients with end-stage liver disease undergoing coronary artery bypass grafting prior to proposed orthotopic liver transplantation. J Cardiothorac Vasc Anesth 1995;9(3): 1-7.
  6. Hadengue A, Benhayoun MK, Lebreg D, Bewhamou JP. Pulmonary hypertension complicating portal hypertension: prevalence and relation to splanchnic hemodynamics. Gastroenterology 1991;100:520-528.
  7. Cheung EY, Woehlck HJ. Pulmonary artery hypertension complicating anesthesia for liver transplantation. Anesthesiology 1992;77:389-392.
  8. Simpson BR, Ramsay MAE, East CA, Sharp JS, Gawey BJ. Pulmonary hypertension in patients needing liver transplantation: review of 1000 patients. Anesthesia Analgesia 1995;80:S469.
  9. Doyle HR, Marino IR, Miro A, Scott V, Martin M, Fung J, et al. Adult respiratory distress syndrome secondary to endstage liver disease — successful outcome following liver transplantation. Transplantation 1993;55:292-296.
  10. Pernambuco JRB, Langley PG, Hughes RD, Izumi S, Williams R. Activators of the fibrinolytic system in patients with fulminant liver failure. Hepatology 1993;18:1350-1356.
  11. Gonwa TA, Poplawski S, Brajtbord D, Goldstein R, Husberg B, Klintmalm GB. Pathogenesis and outcome of hepatorenal syndrome in patients undergoing liver transplantation. Transplant Proc 1989;21(1):2419-2420.
  12. Lebrec D. Current status and future goals of the pharmacologic reduction of portal hypertension. Am J Surg 1990;160:19-25.
  13. Freedman AM, Sanyal AJ, Tisnado J, Shiffman ML, Luketic VA, Fisher RA, et al. Results with percutaneous transjugular intrahepatic portosystemic stent-shunts for control of variceal hemorrhage in patients awaiting liver transplantation. Transplant Proc 1993; 25(1):1087-1089.
  14. Husberg BS, Goldstein RM, Klintmalm GB, Gonwa T, Ramsay MAE, Cofer J, et al. A totally failing liver may be more harmful than no liver at all: three cases of total hepatic devascularization in preparation for emergency liver transplantation. Transplant Proc 1991;23(1):1533-1535.
  15. Ringe B, Pichlmayr R, Lübbe N, Bornscheuer A, Kuse E. Total hepatectomy as temporary approach to acute hepatic or primary graft failure. Transplant Proc 1988;20(1 suppl 1):552-557.
  16. Bakti G, Fisch HU, Karlaganis G, Minder C, Bircher J. Mechanisms of the excessive sedative response of cirrhotics to benzodiazepines: model experiments with triazolam. Hepatology 1987;7:629-638.
  17. Brajtbord D, Parks R, Ramsay MAE, Paulsen AW, Valek TR, Swygert TH, et al. Management of acute elevations of intracranial pressure during hepatic transplantation. Anesthesiology 1989;70:139-141.
  18. Brown BR, Frink EJ. Anesthesia considerations in patients with liver disease. Anesthesiol Rev 1993;20(6):213-220.
  19. Brown MR, Ramsay MAE, Swygert TH. Exchange autotransfusion using the cellsaver during liver transplantation. Anesthesiology 1989;70:168-169.
  20. Lukin C, Hein HAT, Swygert TH, Gunning TC, Valek TR, Donica SK, et al. Duration of vecuronium induced neuromuscular blockade as a predictor of liver allograft dysfunction. Anesthesia Analgesia 1995;80(3):526-533.
  21. Whitten CW, Ramsay MAE, Paulsen AW, Swygert TH, Dyll CM. Upper extremity neuropathy after orthotopic hepatic transplantation: a retrospective analysis. Transplant Proc 1988;20(1 suppl 1):628-629.
  22. Paulsen AW, Whitten CW, Ramsay MAE, Klintmalm GB. Considerations for anesthetic management during veno-venous bypass in adult hepatic transplantation. Anesthesia Analgesia 1989;68:489-496.
  23. Veroli P, El Hage C, Ecoffey C. Does liver transplantation without veno-venous bypass result in renal failure? Anesthesia Analgesia 1992;75:489-494.
  24. Ramsay MAE, Swygert TG. Anaesthesia for hepatic trauma, hepatic resection and liver transplantation. Bailliere's Clinical Anaesthesiology 1992;6(4):863-894.
  25. Greig PD, Woolf GM, Sinclair SB, Abecassis M, Strasberg SM, Taylor BR, et al. Treatment of primary liver graft nonfunction with prostaglandin E1. Transplantation 1989; 48(3):447-453.
  26. Bakker CM, Stibbe J, Gomes MJ, Groenland TN, Metselaar HJ, Hesselink EJ, et al. The appearance of donor heparin in the recipient after reperfusion of a liver graft. Transplantation 1993;56(2):327-329.
  27. Swygert TH, Valek TR, Brajtbord D, Brown MR, Gunning TG, Roberts LC, et al. Effect of intraoperative low dose dopamine on renal function in liver transplant recipients. Anesthesiology 1991;75:571-576.
  28. Takaoka F, Brown MR, Paulsen AW, Ramsay MAE, Klintmalm GB. Adult respiratory distress syndrome following orthotopic liver transplantation. Clin Transplant 1989;3: 294-299.

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