Diagnostic ultrasound ( PDFDrive )

682 PART II Abdominal and Pelvic Sonography
severe grat pancreatitis is associated with a range of complications
akin to those seen in a native pancreas such as pancreatic hemorrhage
and necrosis, peripancreatic luid collections, pseudocysts,
abscesses, and pseudoaneurysms.
Ultrasound can be used to guide aspiration of potential luid
collections and help discriminate pseudocysts from abscesses
or seromas. If infection is demonstrated at the time of ultrasoundguided
aspiration, CT is oten performed to assess the grat in
its entirety and in particular to evaluate for areas of duct disruption
as well as to demonstrate the location of luid collections in
relation to the duodenal C loop and duodenojejunostomy. Early
luid collections are oten surgically managed.
Fluid Collections
Peripancreatic transplant-related luid collections are associated
with an increased likelihood of loss of allograt function and
overall increased mortality and morbidity. Early diagnosis and
characterization of these collections are imperative, because
treatment in the acute stages is associated with improved grat
function and decreased recipient morbidity. 92
In the immediate postoperative period, peritransplant luid
may be caused by leakage of pancreatic luid from transected
ductules and lymphatics, an inlammatory exudate, blood, or
urine (Fig. 18.68). hese collections may require either close
serial imaging follow-up or drainage, depending on the clinical
status of the patient.
Duodenal leaks in systemic venous-bladder drainage
transplants occur from dehiscence of the duodenal-bladder
anastomosis and result in the formation of urinomas, frequently
at the medial aspect of the transplant. Urinomas may also result
from infection or necrosis of the grat. 92
Duodenal leaks in portal venous-enteric drainage transplants
occur at the blind end of the donor duodenum or from the
anastomosis with the recipient Roux-en-Y loop. On ultrasound,
gross ascites, duodenal wall thickening, or free intraperitoneal
air may be observed in patients with breakdown of the duodenal
anastomoses. hese leaks may result in overwhelming sepsis and
can be life-threatening. Furthermore, the presence of digestive
enzymes in contact with the grat may lead to substantial tissue
necrosis. 91
Patients with pancreatic transplants are also susceptible to
infection because of their immunosuppressive therapy, as well
as their underlying diabetes mellitus. Abscesses are occasionally
identiied and are oten associated with hematomas, urinary tract
infections, and pancreatitis. Although gas within a luid collection
may indicate the presence of a gas-forming organism, bubbles
of air within a collection may also result from the presence of
a istula or tissue necrosis in cases of vascular thrombosis.
On sonography these collections may demonstrate a thick
irregular wall with peripheral hyperemia on Doppler interrogation.
If gas is present, it typically is seen as echogenic foci with
posterior reverberation artifact. Adjacent changes in the fat include
increased echogenicity and luid. In the posttransplant period,
the development of a new collection or change in the sonographic
morphology of the collection may result from a variety
of causes, including infection; malfunction of the pancreatic
duct, stent, or external drain; hemorrhage; or associated tissue
infarction. 92
Miscellaneous Complications
Other complications of pancreatic transplants include intussusception
of the Roux-en-Y loop, small bowel obstruction from
adhesions, internal hernias (due to the surgically created mesenteric
defect), and volvulus along the long axis of the grat.
Because the patient is immunocompromised, there is a higher
incidence of entities such as typhlitis or Clostridium diicile colitis.
POST TRANSPLANT
LYMPHOPROLIFERATIVE DISORDER
he global improvement in survival ater transplantation can be
attributed to a parallel improvement in immunosuppressant
regimens. he depressed immune response to oncoviruses such
as the Epstein-Barr virus (EBV) results in increased vulnerability
of these patients to malignancies that are mediated by such
oncoviruses. his contributes to a threefold to eightfold increased
malignancy risk in transplant patients as compared with the
baseline population. 93-95
PTLD is the second most common malignancy in adult
transplant patients, following skin malignancy (nonmelanoma).
96 PTLD encompasses myriad disease processes ranging
from lymphoid hyperplasia to poorly diferentiated lymphoma.
Biopsy is required to discriminate among the various subtypes.
Many patients are asymptomatic or have vague symptomatology,
resulting in a delayed diagnosis. It can be hard to discriminate
PTLD from infection or allograt rejection. Imaging
is therefore important in establishing the diagnosis, enabling
tissue sampling, and monitoring response to treatment.
EBV infection is relatively prevalent, with 90% to 95% of
adults being seropositive; however, most immunocompetent hosts
can eradicate B cells that display EBV antigens by using T cells.
However, in immunocompromised patients as well as a small
group of immunocompetent hosts, a small number of EBVinfected
B cells escape and survive with resultant latent EBV
infection. 97
Ater solid organ transplantation, cytotoxic EBV-speciic T
cells may be completely lost within 6 months of transplantation
as a result of immunosuppressive medication. 98 Latently infected
B cells have the potential to proliferate, resulting in PTLD. 99
A variety of genetic mutations (including p53, NRAS) can
result in PTLD. hese genes are involved in the division, proliferation,
and death of cells. Overproduction of cytokines such as
interleukin-6 has also been implicated in the genesis of PTLD.
Similarly, CMV-seronegative patients have a higher risk of
developing PTLD ater solid organ transplantation. 100
he incidence of PTLD is thought to be related to the degree
of immunosuppression and the type of allograt. he aggressive
immunosuppressive therapy required to prevent heart-lung
transplant rejection has resulted in a reported incidence of PTLD
as high as 4.6%. However, the milder immunosuppression used
in patients with liver transplant or renal transplant has resulted
in a lower incidence of PTLD, reported as 2.2% and 1%,
respectively. 101,102
In addition, the numbers of lymphoid aggregates are higher
in intestinal and lung transplants, both of which are associated
with some of the highest incidences of PTLD. 103 It is therefore