Medical Care of the Liver Transplant Patient

After that, your doctor or a specialist near your home will provide follow-up care.

Laboratory blood tests are obtained twice a week following transplantation. Gradually, the frequency of blood tests will be reduced. You will be notified about any adjustments in your medications.

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Complications can occur with any surgery. Patients undergoing organ transplantation may face additional complications. The life-threatening disease that created the need for your transplant may affect the functioning of other body systems. Other risks, such as rejection, also may occur. Immunosuppressive medications help to prevent and treat rejection.

These drugs decrease your body's resistance to foreign bodies, such as your new liver. You will need to take these medications for the rest of your life or you will reject your liver. Immediately after surgery, the dosages will be high since the probability of rejection is greatest at this time.

Dosages will be lowered quickly to smaller amounts if there are no signs of rejection. The medications have side effects, which are usually dose-related. Most people experience the highest level of side effects in the beginning when medication dosages are high. As the dosage is lowered, these effects will probably lessen. Side effects may occur in some patients and not in others. The etiology and pathophysiology of these intrahepatic strictures have not been clearly elucidated. Often, the strictures seem to be associated with a hepatic artery thrombosis or stenosis, and ischemia of the biliary tree is probably the cause, especially in livers used from non—heart-beating donors.

Preservation damage of the allograft can result in multiple intrahepatic biliary strictures, with or without biliary sludge and casts. In some patients, who originally received transplants for primary sclerosing cholangitis, recurrence of the disease seems a possibility. Although some patients with multiple intrahepatic strictures eventually need retransplant, others can live for years with minimal difficulties, especially if they receive chronic antibiotic prophylaxis. Poor graft function, coagulopathy, imperfect hemostasis, or slippage of a tie can result in postoperative bleeding that requires re-exploration.

Even if easily controlled, postoperative bleeding leads to increased cost, morbidity, and mortality. A possible problem after OLT is fluid retention and the formation of ascites. This is especially more significant in malnourished patients and patients with preexisting ascites and edema.

After ruling out the possibilities of renal dysfunction or vascular problems with the liver, these patients should be managed with diuretics and fluid management. Most patients start mobilizing the extra fluid a week after OLT and then can be treated with diuretic therapy if their kidneys are functioning. Nutritional support and careful management of fluid and electrolyte balance, in addition to diuretic therapy, are essential for treatment. Infection is one of the leading causes of morbidity and mortality in liver transplant recipients.

More than two thirds of liver transplant recipients have an infection in the first year after transplantation, and infection is the leading cause of death in these patients. In addition, the release of cytokines during the infection can have other indirect and negative effects, including allograft injury, opportunistic superinfection, and malignancy.

The risk of infection in liver transplant recipients is determined by the intensity of exposure to infectious agents hospital or community sources and the overall immunosuppression level. This net state of immunosuppression is influenced by dose, duration, sequence, and choice of immunosuppressive medications; underlying immune deficiencies; presence of neutropenia or lymphopenia; mucocutaneous barrier integrity: After OLT, there are three periods during which infections with specific organisms are likely to occur.

During the first period, the first month immediately after transplantation, most infections are related to technical or surgical issues and complications. Exposure to infectious agents through prolonged hospitalization before transplantation or during postoperative care can also result in infection. Bacterial and candidal wound infections, urinary tract infections, catheter-related infections, bacterial pneumonias, and Clostridium difficile colitis predominate during this period; the causative organisms are similar to those for hospital-acquired infections common in other surgical patients.

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Although its incidence has markedly diminished with prophylaxis, reactivated human herpesvirus herpes simplex virus infection can occur in this time frame. The next period is the second through sixth month after transplantation. During this time, infections from opportunistic organisms predominate as a result of cumulative immunosuppression. Viral infections, predominantly cytomegalovirus, and fungal infections, such as those caused by Aspergillus , Cryptococcus , Histoplasma , and Coccidioides species, can occur.

Other herpesviruses, such as varicella-zoster virus, and de novo or recurrent hepatitis B and C viruses can cause infections in this period. Some rare bacterial infections caused by Nocardia and Listeria species, and Mycobacterium tuberculosis infection can also occur. Approximately 7 to 12 months after transplantation, and beyond, most recipients can develop infections such as influenza, urinary tract infections, and community-acquired pneumonias, similar to those acquired by patients who have not received transplants.

Reactivation of human herpesvirus 3 can manifest as herpes zoster, and, although it is uncommon, cytomegalovirus infections can occur. Sinister opportunistic fungal infections can occur as a result of cumulatively high levels of immunosuppression, poor graft function, or heavy environmental exposure. Three notable scenarios can enhance patient susceptibility to opportunistic infections: Acute rejection is an ongoing risk in any solid organ transplant, although it is somewhat less of a risk in OLT compared with more immunogenic organs, such as the kidney. The incidence of rejection varies by type of immunosuppressive agent used and by the patient population.

Increases in bilirubin or liver enzyme levels, or both, after OLT in a stable patient may be the first sign of rejection. Histologic evaluation of the liver allograft liver biopsy is essential for making the diagnosis of rejection. Based on the presence and then the severity of rejection, the patient receives additional treatments, which could range from an increase in the baseline immunosuppressive regimen to the administration of steroid boluses and the addition of other drugs to the maintenance therapy, or the administration of antilymphocyte antibodies in case of resistance to the primary line of therapy.

Early acute rejection does not generally affect patient or graft outcomes for patients not infected with hepatitis C virus HCV , except that multiple acute rejection episodes might be a risk factor for chronic rejection. Many patients with focal or mild histologic signs of rejection on protocol biopsy maintain steady graft function, even without treatment, and many centers no longer treat acute rejection aggressively, particularly in the setting of hepatitis C. Studies have shown a higher relative risk of death for HCV-infected patients with rejection versus that for non—HCV-infected patients with rejection 2.

Therefore, rejection is to be avoided in HCV-infected patients at all times.

Medical Care of the Liver Transplant Patient

Late acute rejection, defined as histologically confirmed acute cellular rejection occurring months after transplantation, can result from a precipitous or marked reduction in immunosuppressive agents or with nonadherence to medication. Chronic rejection is characterized by the destruction of the portal bile ducts or biliary epithelial atrophy, a decreased number of hepatic arterioles in the portal tract, or obliterative arteriopathy. Chronic rejection was once a major cause of liver graft failure; with the newer immunosuppressive agent tacrolimus, the risk of chronic rejection is markedly reduced when used de novo after OLT.

This can even successfully reverse chronic rejection, especially in its early stages also known as rescue therapy when the maintenance immunosuppression does not include tacrolimus. Almost any metabolic imbalance can occur after OLT. This is not surprising, considering the magnitude of the physiologic stress of surgery, fluid shifts, multitude of pharmacologic agents administered, and multisystem complications.

The most common imbalances, however, are hypokalemia, hyperkalemia, hyperglycemia, and hypomagnesemia. Hypokalemia can occur as a side effect of potassium-wasting diuretic therapy, intracellular fluid shifts secondary to metabolic alkalosis, hypothermia, insulin therapy, and corticosteroid therapy.

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Rarely, if the serum potassium level is monitored regularly and supplementation given when indicated, hypokalemia from any cause is significant enough to produce physical signs. Hyperkalemia is more often seen after transplantation, beginning 1 to 2 weeks after OLT. It is caused by renal tubular acidosis secondary to CNI use.

It is easily manageable with a dietary regimen. Rarely, patients need to be placed on mineralocorticoids or potassium- chelating agents. The main cause of hyperglycemia in liver transplant patients is preexisting diabetes mellitus. Other important causes are corticosteroids and CNIs. Drug-induced hyperglycemia is usually transient and improves after discontinuation of steroids and reduction in dosage of CNIs. Hypomagnesemia is another phenomenon after OLT. Many patients are hypomagnesemic from malnutrition before transplantation, and the condition is exacerbated during the postoperative period.

The exact nature of this problem is not completely understood. However, contributing postoperative factors are believed to include diuretic therapy and the renal effects of CNIs. Routine monitoring of the serum magnesium level and supplementation with IV or oral magnesium may be indicated. Patients after transplantation and immunosuppression are prone to develop osteoporosis and other metabolic bone abnormalities.

These patients should be monitored regularly by bone densitometry and other metabolic tests and receive appropriate replacement therapies with oral calcium and bisphosphonates. The wide range of incidence reported could result from the wide disparity in the criteria used to define renal failure and differences in the duration of follow-up.

The most common causative factors include acute tubular necrosis secondary to ischemic or toxic insult to the kidneys, preexisting hepatorenal syndrome HRS or renal insufficiency, diabetes mellitus, drug-induced interstitial nephritis, and CNI nephrotoxicity. Dialysis requirements in the pre- or post-transplantation period, hepatitis C infection, and age have also been variably shown to be associated with an increased risk for the development of chronic kidney disease. In the presence of renal dysfunction after OLT, as the first line of therapy, these agents are withdrawn from the immunosuppressive regimen or the dose is reduced to minimize their nephrotoxic effect.

Many patients with end-stage liver disease can have preexisting renal problems, and in the post-OLT period, CNIs should not be considered as the main cause of renal dysfunction. Careful assessment of patients and the cause of their renal dysfunction possibly performing a renal biopsy is helpful for decision making and for assessing the recoverability of kidney in order to offer appropriate treatment to these patients. In patients in whom significant and prolonged renal dysfunction occurs before OLT, combined liver and kidney transplantation should be considered.

Natients occasionally experience various neurologic problems after OLT. These are more common in adults than in children. Most neurologic complications are related to the degree of pretransplantation encephalopathy caused by hepatic encephalopathy or electrolyte disturbances, in particular hyponatremia, as well as the idiosyncratic central nervous system effects of metabolic abnormalities caused by immunosuppressive agents, most notably the CNIs. These drugs can produce a wide clinical spectrum of signs and symptoms, from mild tremor and acute confusion to status epilepticus.

These could be dose-related and include impaired mentation or confusion, psychosis, dysphasia, mutism, cortical blindness, extrapyramidal syndromes, quadriplegia, encephalopathy, seizures, and coma. Treatment includes reducing or completely discontinuing the suspected offending agent.

Solid organ graft survival rates have improved remarkably since the s because of improved immunosuppression, innovative technical procedures, and assiduous post-transplantation monitoring. However, recipient mortality caused by de novo post-transplantation malignancies remains a serious impediment to long-term survival. The increasing prevalence of post-transplantation malignancies has been evidenced by data collected by transplant registries in the United States, Europe, Australia, and New Zealand, as well as a large single-center analysis.

Various factors have been proposed to explain the increased cancer risk in transplant recipients. Among the earliest was the concept of impaired immune surveillance resulting from systemic immunosuppression. Long-term antigenic stimulation and environmental influences, such as UV irradiation, genetic predisposition, uremia preceding transplantation, donor-and-host interactions, and mutagenic activity of immunosuppressive agents, have also been implicated as potential causative factors.

As might be expected, post-transplantation malignancies are associated with higher mortality rates, and many of the deaths occur in patients with a fully functioning allograft. Post-transplantation lymphoproliferative disorders PTLDs are a heterogeneous group of hyperplasias and lymphomas that are serious post-transplantation complications for all organ recipients.

The clinical signs and symptoms of PTLD are diverse and are similar to those seen during primary EBV infection, such as fever, sweats, malaise, and lymphadenopathy. In contrast to solid organ cancers after OLT, the preponderant risk is in the pediatric population. In any case, it is critical that the local physician and transplantation team search diligently for de novo cancers in OLT patients and, most importantly, educate patients about reducing the risk of cancers by routine use of sunscreens, early testing, and vaccinations. Long-term survival depends on preventing allograft reinfection or slowing disease progression in those who have recurrent disease.

Recurrent infection in the graft can lead to graft failure, retransplantation, or death, and in the past this was the most common cause of reduced patient and graft survival. Significant improvements in patient and graft survival in HBV liver transplant recipients have been made during the past 15 years. The first major therapeutic advance was the use of long-term hepatitis B immune globulin HBIG to prevent reinfection. The second major advance came with the availability of highly effective and well-tolerated antiviral agents against HBV, such as lamivudine, adefovir dipivoxil, and more recently, entecavir and tenafovir, which improved the outcomes of patients with decompensated cirrhosis awaiting transplantation as well as transplant recipients who had recurrent HBV disease.

As a result of these therapies, the outcomes of patients with acute and chronic HBV-related liver disease undergoing liver transplantation are now similar to or better than those of patients undergoing transplantation for non-HBV indications. Because of the increase in development of resistance to lamivudine, the American Association for the Study of Liver Diseases has recommended entecavir for preventing disease recurrence after OLT. Post-transplantation recurrence of HCV infection is a universal phenomenon, with a highly variable natural history.

The histologic progression of chronic hepatitis C is more aggressive and is associated with lower patient and graft survival when compared with that of non-HCV liver recipients. Factors associated with recurrence include donor and recipient age, recipient gender and race, presence of genotype 1, level of viremia at the time of transplantation, the use of strong antilymphocyte induction therapy, and high doses of corticosteroids.

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No single factor has been uniformly shown to be the strongest predictor of outcome. A number of reports have shown no response to histologic improvement. Unfortunately, there are no standard time courses for treatment, dosages, and modes of follow-up. It seems that only prolonged treatment and histologic follow-up can evaluate whether progression of fibrosis is halted following post-OLT treatment for recurrent HCV infection.

Recently, trials with protease inhibitors, alone or in combination with interferon and ribavirin, have shown promising results. Most centers, including our program, start antiviral therapy with interferon and ribavirin in the presence of stage II or III fibrosis in the liver allograft or signs of aggressive recurrence of HCV. During the treatment course, monitoring of platelets, white cell count, hemoglobin, and renal function, in addition to LFTs, is essential. Abnormalities in these tests mandate the dose adjustment of growth factors, such as filgastrim Neupogen and epoetin alfa Epogen.

Recurrence can occur within months after OLT but generally it takes years for the recurrence to occur.

Medical Care of the Liver Transplant Patient | Shafinewaz RPh - www.newyorkethnicfood.com

It can mimic rejection or bile duct complications. Diagnosis is made by appropriate histologic, biochemical, and radiologic tests. Liver transplantation has progressed to become an acceptable means for treating end-stage liver disease, with excellent long-term outcomes. This was not achievable without multidisciplinary teamwork among transplantation center teams and outside primary physicians and caregivers.

Increased understanding of the care of these highly complicated patients and effective communication among team members has benefited these patients, with consequently better long-term functional recovery. Miller, MD John J. Conclusions Summary Suggested Readings. Transfer to an Inpatient Transplantation Unit Following transfer to a designated transplantation inpatient unit, the patient should be closely followed by the surgical and medical team, as well as by pharmacists, nutritionists, and physical therapists.

Discharge Instructions Medications and Prophylactic Measures The maintenance medications after discharge include immunosuppressive agents, prophylactic medications for prevention of opportunistic infections, such as for Pneumocystis jiroveci infection trimethoprim-sulfamethoxazole, or in case of sulfa allergy, dapsone or pentamidine , herpetic infections acyclovir , Candida esophagitis nystatin [Mycostatin] , as well as other prophylactic medications, such as acid-reducing agents proton pump inhibitors, histamine-2 blockers.

Blood Work Instructions Laboratory studies are usually done biweekly for the first 2 weeks, weekly for the next 8 weeks, every other week for 2 months, and then once monthly if laboratory test results are stable. Increased Liver Function Test Results Any dramatic or persistent increase in the results of LFTs mandates a series of diagnostic tests to evaluate for possible causes, such as rejection, ischemic insult to the liver hepatic artery problems , biliary complications, infections viral hepatitis, bacterial sepsis , or drug toxicities or hypersensitivities.

Back to Top Complications and Outcomes The postoperative course in OLT patients ranges from straightforward to extremely complicated, and the outcome depends on the status of the recipient, donor organ, and technical issues in the operation.