In the post operative period several potential complications need to be closely watched for, including the following.
Acute cellular allograft rejection is unlikely to occur within the first few weeks following the transplant, provided immunosuppression is adequate. Subsequently, rejection can occur at any time but is most common in the first year, particularly the first 6 months. Unfortunately, as of yet, there is no single blood test, which will detect an early rejection. Therefore, suspicion of rejection must be based on clinical evaluation. Although no single sign, or combination of clinical signs is entirely reliable, in most instances rejection is associated with fever, a significant increase in stomal output, and GI symptoms such as abdominal pain, cramping, nausea, vomiting and diarrhea.
Although most lab tests are not helpful in confirming the diagnosis, chromium EDTA,23 or Technetium DPTA24 isotope studies have been useful in identifying increased intestinal permeability which correlates well with, but is not specific for, rejection. If rejection is suspected, endoscopic evaluation of the intestinal graft must be performed. The endoscopic evaluation should include as much of the small bowel as possible and biopsies from numerous sites (at least 6) should be obtained, since rejection can often be segmental. The loop ileostomy greatly facilitates this type of assessment and for that reason the ileostomy is usually kept in place for 6 months to a year following the transplant. Although the endoscopic appearance of rejecting small bowel is often abnormal with evidence of inflammation and ulceration, in early rejection it can be quite normal. Zoom-endoscopy appears to provide more a valuable endoscopic identification of acute rejection in the small bowel. The gold standard for diagnosing rejection is histologic evaluation of the biopsies. Typically early rejection is associated with increased apoptotic figures [normal less than 2 to 3 per high power field]. Other histologic findings associated with rejection include: the presence of activated lymphocytes in the lamina propria; loss of goblet cells; loss of villus height, and ulceration.25
When a diagnosis of rejection is made, the patient should be treated with Solumedrol 500mg IV for 3 days. Prograf levels should be rechecked and doses increased accordingly. If there is persistent evidence of rejection following treatment with steroids, the patient should be treated with OKT3 or Thymoglobulin. If, despite maintaining adequate immunosuppressive levels, rejection episodes continue to occur, consideration should be given to adding additional drugs, such as Sirolimus to the immunosuppressive regimen. Because escalation of immuno-suppression can be complicated by life threatening infections or malignancies, such patients should be carefully monitored.
Patients who undergo small bowel transplant are even more susceptible to infectious complications than other transplant recipients. There are primarily two reasons for this:
1. The intestinal allograft is transplanted with a significantly higher load of microorganism than any other organ allograft. Therefore, any process which compromises the intestinal allograft will influence the containment of these microorganisms within the graft and contribute to their spread to various areas of the body.
2. Because intestinal rejection is difficult to detect and because severe rejection can often lead to life threatening sepsis, these patients are maintained on higher degrees of baseline immunosuppression than recipients of other organ transplants.
When bacteria translocate from the compromised intestinal allograft, there are commonly two places where they go initially. Since the lympathics are divided in the procurement of the intestinal allograft it is common that there is leakage of intestinal lymph into the peritoneal cavity. This often contains bacteria. While typically the peritoneal cavity is capable of handling a moderate load of bacteria, in the immunocompromized state—particularly when significant ascites is present—bacterial peritonitis can occur. The second route by which bacteria can spread is by direct translocation into the portal circulation and subsequent dissemination to other sites. Particularly common infections resulting from bacterial translocation are central line infections and pneumonias. The typical organisms are consistent with those, which are found in the GI tract and include E.Coli, klebsiella, enterobacter, staphylococci enterococci, etc. Because of the degree of immunosuppression used, other typical and atypical postoperative infections are more likely to occur.26
A primary concern with intestinal transplantation is the development of a CMV infection, which can manifest as CMV enteritis that can be severe and lead to graft loss. In general, transplantation of a graft from a CMV positive donor to a CMV negative recipient is avoided. The clinical manifestations of CMV enteritis are not unlike that of rejection with fever, increased stomal output and GI symptoms. Other important clues which may sway the clinical diagnosis more towards CMV enteritis include: the CMV status of the donor and recipient, the degree of immunosuppression at the time symptoms developed, and a positive CMV antigenemia assay. Also with CMV infections there is typically a decrease in the white blood cell count and flu-like symptoms. Endoscopy should be performed and multiple biopsies taken if there is a clinical enteritis. While the histologic picture of CMV can sometimes be similar to that of rejection, with CMV enteritis the presence of CMV inclusion bodies is diagnostic. If CMV is diagnosed, the patient should be treated with therapeutic doses of Gancyclovir. If there is evidence of Gancyclovir resistance, Foscarnet or CMV immune globulin (Cytogam) should be considered.
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