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Surgical Complications
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A high incidence of surgical complications can be seen following
intestine transplantation due to the complexity and duration of
the procedure, the history of previous abdominal operations,
and advanced liver disease and suboptimal nutritional status. Complications include,
but are not limited to, intestinal perforation or obstruction, intra-abdominal
bleeding or abscess, wound dehiscence or infection, vascular thromboses,
and stomal prolapse. Allograft volvulus and internal hernia are
important causes of graft obstruction and carry a high risk for
graft loss resulting from ischemia. Reoperation in intestine transplant
recipients ranges from 60% to 90% of cases.
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Infection is not only the leading cause of death in intestine
transplant recipients, but is also the primary diagnosis for readmission during
all periods post transplant. Bacteremia or fungemia often has its
source either intra-abdominally or in relation to long-term vascular
access. In addition to appropriate antimicrobial therapy management
should include the drainage of intra-abdominal collections, or removal
of infected catheters.
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Infectious enteritis may occur in almost 40% of intestinal
transplant recipients; two thirds of the cases being attributable
to viral agents. Adenovirus infections are common and caliciviruses
can also be significant pathogens in this population. Viral pathogens
may cause prolonged but ultimately self-limiting gastroenteritis
but can also cause severe allograft dysfunction post intestinal
transplant. Epstein Barr virus (EBV) is an important cause of viral
illness presenting either as acute infection or as EBV-induced posttransplant lymphoproliferative
disease (PTLD) occurs in about 10% of patients. Treatment
for PTLD in intestinal transplant recipients follows the general
steps outlined in other solid organ transplant recipients; however,
the reduction in immunosuppression has to be done cautiously and
with close allograft monitoring as devastating rejection, even in
the face of active EBV, may occur.
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Causes of acute graft dysfunction include acute cellular rejection,
systemic or abdominal sepsis, infective enteritis, PTLD, and surgical
complications such as intestinal perforation and obstruction. Clinical
manifestations of graft dysfunction include irritability, fever,
vomiting, abdominal distension, and changes in the appearance of
the stoma. Stomal output may be increased, decreased, or bloody
depending on the cause and severity of graft injury. Blood and stool cultures,
viral studies, endoscopy with mucosal biopsy, and radiologic studies
may all be required for exclusion of other causes for symptoms.
Differentiation between viral enteritits and mild acute cellular
rejection may be difficult and experienced pathological interpretation of
the biopsy specimens is essential (see http://tpis.upmc.com).
Viral culture, immunohistochemisty, and in situ PCR may assist with
the diagnosis. A lack of precision with the diagnosis of graft dysfunction
can lead to inappropriate changes in immunosuppression potentially
exacerbating graft injury.
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A standardized system for grading the histologic changes associated
with acute rejection of an intestinal allograft has gained wide
acceptance.5 Changes seen in mild rejection include
multiple apoptic crypt epithelial cells with lymphocytic infiltration.
More severe grades include increased inflammatory cell infiltration,
crypt damage, mucosal architectural alteration, and, ultimately
mucosal loss. The treatment of acute rejection is with intravenous
methylprednisolone boluses (10–20 mg/kg/day)
usually for 3 days and an increase in the background immunosuppression
either by increasing the goal serum levels of tacrolimus or by the
addition of another immunosuppression agent. Endoscopy and biopsy
are repeated frequently to ensure adequate treatment and to document
histological improvement. Antilymphocyte preparations are reserved
for severe or steroid resistant rejection. Severe rejection with
loss of mucosa may necessitate graft enterectomy, particularly if no
regeneration is seen following adequate immunosuppression or if
infection ensues.
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The pathological lesion of chronic rejection is an obliterative
arteriopathy of medium-sized vessels within the transplant mesentery
and deeper layers of the deeper layers of the bowel wall. Mucosal
changes, if present, are nonspecific. Diagnosis requires full thickness
biopsy that is usually available only after enterectomy, when graft
failure is established. Clinical signs of chronic rejection may
include gradually deteriorating allograft mucosal function with
increased ileal or stool outputs or allograft stricture with extensive
submucosal fibrosis. Currently there are no markers of the early
stages of this disease process, and once established, chronic intestinal
allograft rejection does not respond to increased immunosuppression.