Cardiovascular Issues

Hypertension after transplantation is seen in 50-75% of patients in the first weeks and months following surgery. Frequently a patient's essential hypertension is unmasked by correction of his or her hyperdynamic state and worsened by the administration of tacrolimus or cyclosporine. Tacrolimus causes less hypertension than cyclosporine. The additive effect of corticosteroids and calcineurin inhibitors in the exacerbation of hypertension mandates reduction in immunosuppression whenever clinically feasible. Arterial pressure elevations result from increased systemic vascular resistance based on vasoconstriction. Prudent administration of beta and calcium channel blockers usually suffices to correct the hypertension. ACE inhibitors are not recommended in the early postoperative period because renin levels are low at this point. It is important to note that hypertension (and tachycardia) can result from renal dose dopamine.

Hypotension results from falling behind in the resuscitation efforts with intravenous fluids and or blood products. Continued hypotension and transfusion requirements mandate consideration for reexploration. Use of prostaglandin El (PGE1) frequently causes hypotension as well.

Tachycardia may be caused by inadequate pain control, hypovolemia, pulmonary embolus, and dopamine administration.

Bradycardia may result from sick sinus syndrome, infections, overdosage of antiarrhythmics and antihypertensives, and increased intracranial pressures.

Cardiac failure accounts for a 7-21% mortality rate after liver transplantation. Therefore, recognition and proper treatment of cirrhotic cardiomyopathy are essential. Such dysfunction can occur independent of prior alcohol abuse. It may be missed by standard echocardiographic techniques. The liver transplantation procedure, with its attendant hemodynamic and volume shifts, stresses the heart significantly. Acid-base abnormalities, hypothermia, and electrolyte disturbances can also affect myocardial function. As the hyperdynamic physiology of cirrhosis is corrected postprocedure, vasoconstriction causes increased afterload and may precipitate heart failure. Management strategies include diuretics, salt restriction, afterload reduction, and possibly mechanical ventilation. Cirrhotic cardiomyopa-thy may improve after liver transplant.

14.5. HEMATOLOGIC ALTERATIONS

Liver transplant recipients may suffer a number of hematologic adverse events in the immediate postoperative period. Anemia, thrombocytopenia, and neutropenia may result from surgical, infectious, and pharmacologic causes.

Anemia may be dilutional as a result of overaggressive administration of intravenous fluids or inadequate replacement of blood products in the operating room. Continued surgical bleeding occurs in 7-15% of cases and results in reexploration in half of those cases. Other causes of bleeding include ulcers, viral enteritis, portal hypertensive lesions, and Roux-en-Y bleeds. Therefore, aggressive diagnostic and therapeutic maneuvers are crucial in the early postoperative period. These include upper and lower endoscopy, bleeding scans, angiograms, and reexploration. It is imperative that medical coagulopathy be corrected judi ciously. Ulcer prophylaxis is usually adequate with proton pump inhibitors. Var-iceal bleeds may result from a thrombosed hepatic artery or portal vein.

If the hemoglobin is too high (particularly in pediatric patients), therapeutic phlebotomy may be necessary to prevent vascular thrombosis.

Thrombocytopenia may result from continued splenic sequestration, drug toxicity (furosemide, mycophenolate), infections (herpes, parvovirus, sepsis syndrome), preformed antibodies, and rejection. Usually it is safe to allow a platelet count of 20,000 as long as there is no bleeding. With a well-functioning graft, thrombocytopenia should resolve within 1 week.

Neutropenia may result from drug toxicity (mycophenolate and rapamycin) and infections as well. The treatment is aimed at the inciting agent. Neupogen® is sometimes given when the counts are low.

Elevated white blood cell counts usually signal ongoing infection but may just reflect steroid effect.

Coagulopathy seen in the cirrhotic frequently persists postoperatively. If the patient is not bleeding and/or the prothrombin time seconds, cautious observation is recommended. In the face of bleeding or higher PT, prudent administration of factors such as fresh-frozen plasma and cryoprecipitate (if the fibrinogen is lower than 100) may be necessary.

14.6. INFECTIONS IN THE IMMEDIATE POSTOPERATIVE PERIOD

Mortality related to infection in liver transplant recipients is 10%. Because of immunosuppression, anergy, and malnutrition, infected liver transplant patients do not present with classic findings. Not infrequently a recipient may be infected and not demonstrate an elevated white blood cell (WBC) count or fever. In a recent study, 23% of all infections were unaccompanied by fever and 9% were accompanied by hypothermia. Bile peritonitis may be present in a patient with a soft, nontender abdomen. It is therefore imperative to have a high index of suspicion. A pulmonary infiltrate, with or without fever or elevated WBC, is likely to be pneumonia. Greenish output from an abdominal drain is bile peritonitis until proven otherwise, regardless of temperature or physical examination. Additionally, those patients who do have fever in the ICU are very likely (87%) to have infection. In the ICU, 79% of infections are bacterial, 9% viral, and 9% fungal. In all liver transplant recipients, 55% of infections are bacterial, 22% fungal, and 22% viral. Over half of bacterial infections occur in the first two postoperative weeks, which is the time of greatest immunosuppression. The etiology of most bacterial infections is usually Gram-positive bacteria. Treatment is based on isolation of the offending organism, surgical or percutaneous drainage when appropriate, and proper antibiotic coverage. Risk factors for bacterial infection are extremes of age, malnutrition, prolonged hospital stay, prolonged operative time, increased blood transfusions, and surgical complications such as hepatic artery thrombosis and biliary obstruction or leak. Prophylaxis is targeted at Gram-positive organisms such as staphylococcal and enteric bacteria. Ampicillin or Piperacillin are frequently employed for 2-7 days postoperatively. In penicillin-allergic patients, Vancomycin is frequently used with a second- or third-generation ceph-alosporin.

Fungal infections occur most commonly in the first 8 weeks after transplantation. Risk factors are similar to those for bacterial infection. Candida is the most frequent culprit. Treatment is with amphotericin or its liposomal formulations, or fluconazole. Prophylaxis in high-riskpatients may be warranted. However, excessive use of fluconazole prophylaxis has led to the emergence of resistant strains. Aspergillus accounts for approximately 15% of all fungal infections and is responsible for 90% of brain abscesses. Treatment is with amphotericin and/or itraconazole. There are studies evaluating the utility of itraconazole prophylaxis. No benefit has been shown.

Pneumocystis carinii is a parasite infection that usually affects patients late after transplantation. Prophylaxis is with trimethoprim-sulfamethoxazole. Data support its use for at least 1 year.

Most viral infections occur between 3 and 4 weeks postoperatively. However, up to 10% of infections in the immediate postoperative period are viral in nature. Reactivation of cytomegalovirus (CMV) is a major cause of viral infection. CMV syndrome is manifested by fever, myalgia, malaise, leukopenia, and thrombocytopenia. The liver allograft is the most common site of organ involvement. Treatment and prophylaxis with immune globulin preparations, gancyclovir (IV and by mouth), and/or acyclovir are extremely effective. This regimen should last approximately 100 days.

14.7. PRIMARY GRAFT NONFUNCTION (PNF)

PNF is the most common cause of graft loss in the immediate postoperative period. It is generally defined as immediate perioperative graft failure with coagulopathy, acidosis, hypothermia, encephalopathy, decreased bile output, and elevated liver function tests. The incidence ranges between 2% and 10%. The risk factors include, but are not limited to, advanced donor age, steatosis, and prolonged cold and warm ischemia time. Ischemia-reperfusion injury, free radical production, leukotrienes, thromboxanes, other immune-mediated events, and possible metabolic derangements, all may play a role in its pathogenesis. Early PNF may improve with supportive care or with the administration of PGE1. Unfortunately, retransplantation is the only option for patients who remain encephalopathy, acidotic, hypoglycemic, hypothermic, and coagulopathic. A liver biopsy with greater than 50% necrosis confirms the diagnosis but is unreliable and rarely performed. If a liver does not become available, hepatectomy with portocaval shunting or continuous bypass may become necessary until a proper donor is identified.

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