Keywords
interventional radiology - pancreatic cancer - pancreatic transplant - pancreatitis
- peripancreatic collection
Introduction
Approximately 20% of patients with acute pancreatitis will develop complications that
require intervention.[1] These can be classified into vascular and nonvascular complications[2]:
-
Nonvascular complications include collections, bowel complications, and pancreatic
fistulas.[2]
-
Vascular complications include peripancreatic arterial and venous pseudoaneurysms,
venous thrombosis, and arteriovenous malformations (AVMs).[3]
Pancreatic adenocarcinoma is the 12th most common malignancy and the 7th leading cause
of cancer-related mortality globally.[4] Most patients present late with either locally extensive or metastatic disease.[5] The aggressive nature, late presentation, and lack of effective therapies all contribute
to the poor prognosis. Patients with more advanced disease will typically undergo
either endoscopic ultrasound (US) or interventional radiology-guided interventions
to deliver either palliative or preoperative care.[4]
Pancreas transplantation offers diabetic patients the prospect of glycemic control
free of exogenous insulin administration, with a significant improvement in quality
of life and reduction in diabetes-associated complications.[6] Surgery can, however, be complicated by a high rate of early technical failure.[7] Percutaneous and endovascular interventions are increasingly performed for the diagnosis
of rejection and the treatment of vascular complications.
Nonvascular Interventions
Nonvascular Interventions
Drainage of Peripancreatic Collection
Intra-abdominal collections and abscesses are the most common complication following
acute pancreatitis.[8] Collections are classified according to the revised Atlanta Classification into
acute peripancreatic fluid collections, pseudocysts, acute necrotic collections, and
walled-off pancreatic necrosis[9]
[10] ([Fig. 1]). Symptomatic intra-abdominal collections require imaging-guided drainage. When
a collection is readily visualized on US, US-guided percutaneous drainage placement
is generally the preferred choice as US is less expensive, allows for real-time monitoring
of the needle placement, and is free from ionizing radiation.[11] However, the combination of US and fluoroscopy can improve on this by facilitating
safe needle puncture using US guidance followed by optimal drain positioning using
fluoroscopic guidance.
Fig. 1 (A) Acute peripancreatic fluid collection (green arrow). (B) Multiple pseudocysts (yellow arrows) in the context of acute on chronic pancreatitis
(note the pancreatic calcifications). (C) Acute necrotic collection (note absent enhancement of the pancreatic head). (D) Percutaneously drained walled-off necrosis (blue arrow indicate the wall). (E) This had been subsequently infected (note the presence of gas).
Infected pancreatic necrosis is often poorly marginated and nonenhanced and may contain
bubbles of gas. However, these features are not always present, and necrotic collections
without signs of infection at CT should be considered sterile until proven otherwise.
Percutaneous drainage is generally avoided in this context due to the potential risk
of introducing infection. Deteriorating patients with high clinical suspicion of infection
may benefit from US-guided aspiration to rule out an infected pancreatic necrosis.
When infected necrosis is present, large-bore or multiple percutaneous drainage catheters
should be sited in the collection as a bridge or as an alternative to surgical debridement.[12]
Guidelines from 2013 by the International Association of Pancreatology and the American
Pancreatic Association advise postponing all forms of invasive intervention in patients
with infected necrosis, preferably until 4 weeks after the onset of disease.[13] The rationale behind this is fourfold. First, antibiotics alone might be sufficient
as treatment. Second, diagnosing infected necrotizing pancreatitis is often easier
in the later stages of the disease, when all other sources of infection or systemic
inflammatory response have been ruled out. Third, catheter drainage is typically easier
once the collection has become more liquefied and the stage of walled-off necrosis
has been reached. Fourth, endoscopic transluminal drainage requires a walled-off collection.
In theory, it is not always necessary to wait several weeks until full encapsulation
of peripancreatic collections and percutaneous drainage can be performed safely and
successfully in the first weeks after the onset of disease.[14] If there is no technical reason for postponing catheter drainage, patients with
infected necrotizing pancreatitis might benefit from earlier catheter drainage in
terms of reducing the rate of complications and length of hospital stay. This is also
the case in the context of abdominal compartment syndrome. More recently, the Dutch
Pancreatitis Study Group is undertaking a randomized controlled trial (POINTER [postponed
or immediate drainage of infected necrotizing pancreatitis]) that will compare immediate
and delayed catheter drainage in an attempt to further improve the outcome of these
severely ill patients.[15]
When a collection is located deep in the abdomen or is poorly visualized on US, computed
tomography (CT) offers adequate guidance to allow safe placement of percutaneous drains.[16]
After placement and aspiration of fluid, self-locking pigtail drains of size 8 to
12 Fr are left in place and irrigated with 10 to 20 mL of sterile saline three times
daily. Catheters can be upsized to a maximum of 28 F, as the clinical situation evolves
if smaller drains prove inadequate.[8]
External drainage of peripancreatic collections may fail in the setting of abnormal
pancreatic ductal anatomy. In a study by Nealon et al, there was a statistically significant
difference in successful percutaneous drainage between patients with normal pancreatic
duct anatomy and those with a pancreatic duct stricture or duct disconnection.[17] Drainage failed to permanently resolve the collection in half of the patients with
duct strictures and was uniformly unsuccessful in patients with ductal disconnection
or occlusion.
The incidence of cyst–cutaneous fistula formation is reportedly as high as 50% in
certain settings[18]; therefore internal transgastric drainage is preferable in situations in which a
persistent pseudocyst is being driven by a persisting pancreatic duct fistula ([Fig. 2]).
Fig. 2 CT-guided drainage of peripancreatic collection through a right posterior approach.
Pseudocyst Gastrostomy
Iatrogenic communication between a pseudocyst and hollow viscus can be formed to enable
drainage ([Fig. 3]). Internal gastric drainage of pancreatic pseudocysts is now commonly performed
under endoscopic US guidance.[19] CT-guided percutaneous technique cannot regularly provide an adequately wide cystogastrostomy
opening.[11] Surgical cystogastrostomy is usually reserved for necrotic collections that do not
abut the gastrointestinal tract and may be found in the retroperitoneal space.[19]
Fig. 3 (A, B) Coronal and axial maximum intensity projection reformatted CT (computed tomography)
showing pseudocyst gastrostomy.
The percutaneous approach typically necessitates two stages, with the pseudocyst initially
being drained percutaneously through a transgastric route as a temporary bridge before
converting into an internal cystogastrostomy drainage through a double-J stent or
by pushing the percutaneous drain into the stomach.[20]
There is no consensus about the duration of drainage through pseudocyst gastrostomy.
After the introduction of this technique in 1984, pigtail catheter removal was initially
advised after 3 months. The technique has since evolved such that the catheter is
left in situ for at least 1 year to more than 3 years if there is a concern that catheter
removal would lead to symptomatic recurrence. Catheter removal by forceps during routine
gastroscopy in the outpatient setting has been reported.[21]
Technical success in percutaneous catheter placement is greater than 90%, with an
immediate complication rate of around 6% and a mortality rate of 1%.[18] Secondary infection with abscess formation is not uncommon, occurring in around
11%.[21] Complete resolution of the pseudocyst with this method has been reported in at least
88% of cases.[18]
Fistula Treatment
Pancreatic fistulas may complicate pancreatic surgery or necrotizing pancreatitis.[22] They can communicate with bowel loops, liver, or other adjacent viscera.[23]
The incidence of gastrointestinal fistulation following acute pancreatitis is reportedly
3 to 47%, with an associated increase in mortality of up to 34.7% in those with pancreatic
colonic fistulae.[24]
In the presence of a fluid collection, percutaneous drainage can treat the collection,
and this may occasionally lead to spontaneous resolution of the fistula.[16] If the main component of a fistula is of biliary origin, transhepatic biliary drain
insertion can lead to fistula closure by diverting bile from the site of the fistula.
In cases with persisting biliary leak, the placement of an occlusion balloon above
the fistula may divert biliary flow away from the fistula.[25]
Direct fistula embolization has been found to be effective, with access gained through
the tract of a previous surgical drain, through an image-guided percutaneous drain,
or through a transhepatic approach. Once the fistula site has been reached, different
materials may be used to facilitate closure, including ethanol, particles, or glue.[16]
[26]
Percutaneous Necrosectomy
Following liquefaction and encapsulation of necrotic pancreatic tissue, persistent
infection of these cavities despite percutaneous drainage has been ascribed to the
formation and infection of sequestered solid necrotic tissue that is presumed to be
inaccessible to antibiotics.[27] Surgical necrosectomy has historically been the mainstay of treatment for symptomatic
patients.[28] However, in the current era, when percutaneous or endoscopic drainage of pancreatic
abscess/infected necrotic collection fails, there may be a role for percutaneous necrosectomy
in patients who are not fit for open or laparoscopic drainage.[27]
The procedure is performed by exchanging a preexisting left flank drain for a guidewire.
Right-sided or transperitoneal drainage is also possible.[29] A low-compliance balloon dilator is inserted into the collection and dilated to
up to 30 Fr. Access to the cavity is achieved by passing a nephroscope (or similar)
through a sheath, which allows debridement under direct vision. The nephroscope has
an operating channel that permits standard (5 mm) laparoscopic graspers as well as
an irrigation/suction channel. High-flow lavage promotes initial evacuation of pus
and liquefied necrotic material, exposing residual black or gray devascularized pancreatic
necrosis and peripancreatic fat, which, if loose, is extracted in a piecemeal fashion
until, after several procedures, a cavity lined by viable granulation tissue is created.
At the end of the procedure, an 8-Fr catheter sutured to a 24-Fr drain is passed into
the cavity to allow continuous postoperative lavage of warm 0.9% normal saline.[29] Chemically assisted debridement with hydrogen peroxide has been reported during
endoscopic drainage.[30]
The necrotic pancreatic body and fatty tissue can also be fragmented using a snare
catheter (LASSOS, Osypka Medical, Rheinfelden, Germany) and a Dormia basket advanced
through the percutaneous sheath.[27] Others described the use of a 14- to 16-Fr Malecot catheter (CR Bard Inc., Covington,
Georgia) for debridement by twisting it repeatedly inside the collection. An endoscopic
clamp through an appropriately sized introducer sheath can also be used percutaneously
for the same purpose.[31]
Vascular Interventions
Endovascular Treatment of Bleeding
Peripancreatic Pseudoaneurysm Embolization
Pseudoaneurysms develop in approximately 4 to 8% of patients with chronic pancreatitis
and less frequently in the context of acute pancreatitis.[32]
[33] They most commonly affect the splenic artery followed by gastroduodenal, pancreaticoduodenal,
and hepatic arteries.[34]
The etiology is attributed to an enzymatic insult to peripancreatic arteries or erosion
of a pseudocyst into adjacent visceral arteries. Although rupture of a pseudoaneurysm
is rare, it is a serious complication, potentially resulting in massive hemorrhage
with concomitant significant clinical deterioration. A mortality rate of up to 37%
has been reported.[35]
Early detection of pseudoaneurysms is important to prevent subsequent rupture and
catastrophic outcomes ([Fig. 4]). Abdominopelvic CT is the imaging modality of choice in patients with complicated
pancreatitis. Images are obtained following intravenous administration of 100 to 150
mL of iodinated contrast material at a rate of 3.5 mL/second or higher using a mechanical
power injector. Craniocaudal pancreatic scanning is performed during breath-hold and
commenced 30 to 50 seconds from the start of the contrast injection (pancreatic parenchymal
phase). This imaging technique is suitable for the detection and follow-up of nonvascular
complications of pancreatitis, as well as venous and most arterial complications.
Detection of more subtle arterial complications (small pseudoaneurysms and subtle
arterial hemorrhage) may require confirmation with CT angiography or catheter angiography
in indeterminate cases.[36]
Fig. 4 A 48-year-old man with a peripancreatic collection as a sequel of acute pancreatitis
was treated with a percutaneous drain (yellow arrow). Follow-up CT (computed tomography)
during his admission revealed a splenic artery pseudoaneurysm, which was overlooked
at the time of scanning (blue arrow). A few days later, the pseudoaneurysm ruptured
and the patient presented with massive fresh rectal hemorrhage. As displayed in (B), The left flank drain has eroded its way into the descending colon, with side holes
inside and outside the bowel.
Several techniques for the endovascular treatment of pseudoaneurysms have been reported
in the literature using various embolization agents, such as embolization of the aneurysm
neck, embolization proximal to the pseudoaneurysm, and embolization of vessels both
distal and proximal to the pseudoaneurysm, the so-called “isolation” or “sandwich”
technique.[37]
[38]
[39] Preference for a specific therapeutic approach must take into consideration several
factors such as the anatomical location of the affected vessel, the nature of the
artery (expendable with extensive collateral circulation vs. nonexpendable), the size
of pseudoaneurysm sac, and the patient’s hemodynamic status.[33]
Although embolization of the aneurysmal neck can spare blood flow in the parent artery,
infusion of the embolization material may induce rupture due to the fragility of the
aneurysm wall.[40] In addition, this technique increases the risk of migration of embolic materials.[41] Embolization at a point proximal to the pseudoaneurysm is generally a more straightforward
technique but carries a higher risk of failure secondary to blood flow from collateral
vessels. It is for this reason that the isolation technique using aneurysm coils is
considered the optimal endovascular approach in patients with visceral artery pseudoaneurysms.[42]
In a series of 37 patients with visceral artery pseudoaneurysms embolized with coils
using the isolation technique, 32 patients had confirmed complete resolution of pseudoaneurysms
on CT scans obtained at 1 day postprocedure, although two cases of recurrence were
seen during follow-up.[42]
Several recent studies have reported the effectiveness of transcatheter arterial embolization
with N-butyl cyanoacrylate (NBCA) glue.[43]
[44] According to Toyoda et al, the hemostasis ratios for acute gastroduodenal bleeding
treated by transcatheter arterial embolization with NBCA and transcatheter arterial
embolization with gelatin sponge particles and/or coils are 85.7 and 78.3%, respectively.
When the isolation technique cannot be performed, NBCA embolization is recommended
as an alternative.[40]
Stent grafts can be used to exclude pseudoaneurysm if the neck is unfavorable or when
the parent artery is nonexpendable (e.g., the superior mesenteric artery [SMA]).[33]
Bovine thrombin is also an option as an endovascular embolic agent. Although an off-label
use of the thrombin, it has also been used for percutaneous direct puncture and embolization
of pseudoaneurysm by injecting thrombin into the pseudoaneurysm as well as the surrounding
fluid collection percutaneously under CT guidance.[45]
[46]
Other materials used for percutaneous direct puncture for pancreatitis-related pseudoaneurysm
treatment include glue,[47] Gelfoam,[43] PVA (polyvinyl alcohol) particles,[48] and coils,[48] with variable success rates.
If there is a concern that high-velocity blood flow will increase the risk of nontarget
embolization when using liquid embolic agents and coils, vascular occlusion plugs
may be useful, providing a well-controlled and stable occlusion. Vascular occlusion
plugs also have the advantage of having a more flexible delivery system when compared
with stent grafts, and recent advances in technology have seen the introduction of
plugs deliverable through a microcatheter.[33]
Overall, transarterial embolization of pancreatitis-related pseudoaneurysms is relatively
safe and effective. Recurrence or new pseudoaneurysm formation rates are low and usually
occur within 6 months of embolization.[49]
Venous pseudoaneurysms are an extremely rare complication of pancreatitis, with a
handful of known cases following pancreatic surgery or abdominal trauma.[50]
[51] Spontaneous resolution has been reported, with a natural progression to thrombosis.
In another case, a posttraumatic superior mesenteric vein pseudoaneurysm was treated
with coiling through a percutaneous transhepatic approach.[51]
Ruptured Pseudoaneurysm into a Pseudocyst (Hemosuccus Pancreaticus)
A peripancreatic pseudoaneurysm may rarely rupture into a pancreatic pseudocyst, with
hemorrhage traveling through the pancreatic duct into the gastrointestinal tract through
the ampulla of Vater ([Fig. 5]). This condition, “hemosuccus pancreaticus” (HP), was first reported by Sandblom
in 1970, with an estimated incidence of 1 in 1,500 cases of acute gastrointestinal
hemorrhage.[52]
Fig. 5 Coronal reformatted CT (computed tomography) in (A) arterial and (B) portal venous phases in an 89-year-old male patient with massive upper gastrointestinal
(GI) hemorrhage. There is evidence of rupture of splenic artery pseudoaneurysm (yellow
arrow) into a pancreatic tail pseudocyst (blue arrows). The GI hemorrhage was presumed
to be coming from a pseudocyst eroding through the stomach (green arrow). (C,D) This was treated successfully with coil embolization of the splenic artery.
The most common cause of HP is chronic recurrent pancreatitis related to chronic alcoholism,
which results in pancreatic pseudocyst formation.[53] The peripancreatic vessels most commonly involved are splenic, gastroduodenal, pancreaticoduodenal,
gastric, and hepatic arteries.[54]
The most common symptoms are melena and upper abdominal pain. Visualization of spurting
blood from the ampulla of Vater is diagnostic.[55] However, because of the typically intermittent nature of the bleeding, and difficulty
visualizing bleeding from the ampulla of Vater using an end-viewing endoscope, upper
gastrointestinal endoscopy establishes the diagnosis in only 30% of cases.[56] Diagnosis can often be challenging with only a suspicion of a pseudoaneurysm on
cross-sectional imaging. Treatment approach is similar to other peripancreatic pseudoaneurysms.
Hemorrhagic Pseudocysts
As previously described, pseudoaneurysms can be free-standing or can be located within
a pseudocyst. Furthermore, pseudocysts can erode into an adjacent artery, forming
an expanding hemorrhagic cyst that can rupture into an adjacent hollow organ, or can
communicate with the pancreatic duct producing HP.[32]
The overall incidence of bleeding associated with pancreatitis is not well established.
The prevalence of bleeding pseudocysts ranges from 2 to 31%.[32]
[57] While most life-threatening hemorrhage is arterial in origin, venous bleeding can
occur, as well as massive diffuse small vessel hemorrhage associated with pancreatic
necrosis.
Spontaneous abdominal hemorrhage can develop at any time in patients with a history
of pancreatitis but is often a late complication, with a mean time of occurrence of
2.3 years.[32] In Balthazar and Fisher’s series of 16 patients with pancreatitis-related hemorrhage,
bleeding was secondary to pseudoaneurysms in 61%, hemorrhagic pseudocysts in 19.5%,
and severe capillary and venous bleeding associated with pancreatic necrosis in 19.5%.
It is not always possible to identify a single culprit vessel on CT or angiography;
hence, surgical treatment is suggested in case of severe venous or diffuse capillary
bleeding, hemorrhagic pseudocysts, and unsuccessful embolization ([Fig. 6]).
Fig. 6 A 28-year-old male with previous gallstone pancreatitis underwent a follow-up MRI
(magnetic resonance imaging) for a known pseudocyst. (A) Coronal FIESTA (fast imaging employing steady-state acquisition) sequence demonstrates
isointense material within pancreatic pseudocyst suspicious of hemorrhage. (B) Arterial phase coronal CT (computed tomography) shows high-density material within
the cyst in keeping with hemorrhage; however, no pseudoaneurysm was seen. The patient
underwent catheter angiography, which did not reveal a site of active contrast extravasation
or a pseudoaneurysm (not shown).
Pancreatic Arteriovenous Malformation Embolization
Pancreatic AVM (P-AVM) is rare (~90 cases have been reported).[58] They may be congenital in association with hereditary hemorrhagic telangiectasia
or Osler–Weber–Rendu’s disease. They may also be posttraumatic or occur following
pancreatic transplantation, neoplasm, or inflammation.[59]
The majority of patients with P-AVM remain asymptomatic. Gastrointestinal hemorrhage
may occur from a ruptured varix secondary to portal hypertension or direct erosion
of the AVM into the pancreatic/bile duct or through the adjacent intestinal mucosa
as a duodenal ulcer.[58]
The pancreatic head is most commonly involved (56%) followed by the body and tail
(33%), with the entire pancreas involved in 7%. The definitive treatment for P-AVM
has traditionally been surgical resection.[60] However, Bruno et al described a case of a P-AVM communicating the splenic artery,
the superior pancreatic artery, and the splenic vein.[61] This was treated with coil embolization of the two feeding arteries, with no significant
filling of the portal vein on subsequent angiography.
Oncological Interventions
Oncological Interventions
Percutaneous Biopsy
Biopsy can be performed intraoperatively, endoscopically, or percutaneously with CT
or US guidance.[62] Percutaneous imaging-guided fine needle aspiration (FNA) has been in use since the
1970s, but it can be challenging to establish a definitive diagnosis of pancreatic
adenocarcinoma from cytology samples. As an alternative, image-guided percutaneous
biopsy of the pancreas with an automated core biopsy needle has become more commonly
used.[63]
A retrospective study by Yang et al reviewed a sampling of 88 pancreatic masses: 13
underwent FNA only, 60 underwent core needle biopsy only, and 15 underwent both.[64] The diagnostic accuracy of core biopsy alone and both core biopsy and FNA was comparable
at 93.3% and was marginally lower for patients who underwent FNA alone (92.3%). The
negative predictive value was 57% overall for all biopsies. This is too low for a
reliable exclusion of the presence of pancreatic malignancy and suggests that negative
results of percutaneous biopsy, whether core or FNA, should be viewed with caution.
Percutaneous Transhepatic Biliary Drainage
Malignant biliary obstruction is most commonly associated with pancreatic carcinoma,
developing in 70 to 90% of patients and typically leading to jaundice, pruritus, hepatocellular
dysfunction, malabsorption coagulopathy, and cholangitis.[65] Biliary decompression may be achieved by endoscopic retrograde cholangiopancreatography
(ERCP) or through percutaneous transhepatic biliary drainage (PTBD).
Endoscopic insertion of plastic or metal stents is technically successful in approximately
90 to 95% of malignant biliary obstruction cases.[66] If ERCP fails due to inaccessible papilla due to congenital or surgically altered
anatomy, failed cannulation, or the presence of severe tumor-induced stricturing of
the bile duct and/or duodenum, PTBD can be undertaken[4] ([Fig. 7]).
Fig. 7 (A) Coronal reformatted CT (computed tomography) demonstrates pancreatic head tumor
(yellow arrow) causing biliary tree dilatation (blue arrow). (B) This was treated with percutaneous transhepatic biliary drainage.
An intrahepatic bile duct branch is accessed (under fluoroscopic and/or US guidance)
with an 18- to 22-gauge needle followed by a 0.018-inch guidewire. Puncture with a
smaller caliber (22-gauge) needle has been shown to be safer in patients without intrahepatic
bile duct dilatation.[4] Intraductal position is confirmed by a backflow of bile or by fluoroscopic visualization
of injected contrast. The 0.018-inch guidewire is exchanged for a 0.035-inch guidewire.
Depending on operator preference, an access sheath (generally 6 Fr or larger) may
be used and the stricture crossed using a catheter and guidewire. After crossing the
stricture, the wire is exchanged for a stiff wire. The drainage catheter or stent
is then deployed. Internal/external drains must have side holes on each side of the
obstruction but not extending into the liver parenchyma as this leads to bile leak.
Stents must completely cover the lesion.
Drainage is successful in approximately 95% of patients with dilated intrahepatic
bile ducts but only 70% of patients with nondilated ducts.[67]
Results from a national audit of 833 patients in the United Kingdom who had undergone
PTBD in 2009 showed high immediate technical success for drainage and stenting (>95%).
Minor complications occurred in 26.0% of patients, the most common being pain (14.3%),
sepsis (7.7%), and hemorrhage (4.5%). Major complications occurred in 7.9% of patients,
the most common being hemorrhage (3.5%), renal failure (1.8%), and sepsis (1.6%).[68] Data also showed a high inhospital mortality rate (19.8%) in patients with malignancy.
However, this high mortality cannot be entirely attributable to the procedure and
is considered to most likely reflect the underlying disease and multiple comorbidities
in this patient group.[68] Mortality attributed to percutaneous biliary tract interventions alone is much rarer
and ranges from 0.1 to 0.8%.[69]
Ablative Therapies
Experience and data with pancreatic tumor ablative therapy are regarded as investigational
and limited.[4] Brachytherapy delivered by a percutaneous approach has been found to be minimally
effective. Other endoscopic ablative therapies have been trialed, including endoscopic
fiducial markers and brachytherapy, photodynamic therapy, EUS-guided radiofrequency
ablation (RFA), and EUS-guided alcohol ablation.[4] We will focus on other nonendoscopic percutaneous interventions including percutaneous
RFA, microwave ablation, irreversible electroporation (IRE), and electrochemotherapy
(ECT). Their current role in the treatment of pancreatic cancer is still under investigation.
Radiofrequency Ablation
Wu et al first described open surgical RFA for unresectable pancreatic tumors.[70] Sixteen patients with unresectable pancreatic cancer were treated by open cool-tip
RFA, a with high mortality rate (25%) due to dramatic direct portal venous gastrointestinal
hemorrhage and acute renal failure.
In a later study by Girelli et al, 50 patients with locally advanced pancreatic cancer
underwent US-guided RFA during laparotomy.[71] RFA was the only treatment in 19 patients. RFA was combined with biliary and gastric
bypass in 19 patients, gastric bypass alone in 8, biliary bypass alone in 3, and pancreaticojejunostomy
in 1. There was only one case of 30-day mortality in this series. The reported RFA-related
complications were two cases of pancreatic fistulas and four cases of portal vein
thrombosis.[71]
Microwave Ablation
High-frequency (2.45-GHz) microwave ablation (MWA) for the treatment of unresectable
and nonmetastatic locally advanced pancreatic cancer has been trialed by Lygidakis
et al.[72] It has been suggested as a local effective procedure that is feasible and safe,
with acceptable minor complications in locally advanced pancreatic tumors, which can
be used as part of a palliative or multimodality treatment.
However, the feasibility and safety of percutaneous MWA approach require further evaluation.[72]
Percutaneous Irreversible Electroporation
This is a nonthermal ablative technology first described in 2009 by Garcia et al.[73] It uses high-voltage low-energy direct current through electrodes placed into the
pancreas percutaneously under CT guidance to create permanent pores in the cell membrane,
leading to cell death.
The largest retrospective review of patients with pancreatic adenocarcinoma who underwent
percutaneous IRE was conducted at Miami Cancer Institute in 2014.[74] The study included 50 patients with biopsy-proven unresectable pancreatic cancer.
The overall survival for the entire cohort from the date of IRE was 14.5 months (95%
confidence interval: 10.4–18.6 months). Complications occurred in 20% of patients,
including pancreatitis, pain, sepsis, and gastric leak.
Electrochemotherapy
ECT is an electroporation-based therapy with an already established place in the treatment
of cutaneous and liver tumors.
Only one case series (clinical phase I/II) of intraoperative pancreatic ECT with 13
patients has been reported.[75] Intraoperative electrodes were inserted with US guidance into and around the tumor
followed by an intravenous bolus of bleomycin (15,000 IU/m[2]) and subsequent electric pulses by an electric pulse generator. Treatment was completed
within the time window of 8 to 28 minutes after the end of the bleomycin bolus. This
time window ensured the maximum concentration of drug within the lesion. No intra-
or postoperative serious adverse events related to ECT were observed.[75]
Further research is being undertaken to evaluate the safety and efficacy of this technique
in pancreatic cancer treatment.[76]
Interventional Radiology for the Transplanted Pancreas
Interventional Radiology for the Transplanted Pancreas
Pancreas transplantation is most frequently performed in conjunction with kidney transplantation
in the cases of end-stage renal failure secondary to type 1 diabetes. This procedure
is known as simultaneous pancreas–kidney transplantation.[1]
The pancreas allograft and a short segment of duodenum are typically placed intraperitoneally
in the right side of the abdomen, with the donor kidney generally placed in the left
iliac fossa. A donor iliac artery Y-conduit is anastomosed between the SMA and splenic
artery of the graft and the common or external iliac artery of the recipient. The
venous outflow of the pancreas graft may be drained either systemically into the recipient
inferior vena cava or by end-to-side anastomosis from the donor portal vein to the
recipient common or external iliac vein.
The pancreatic exocrine enzymes can be drained directly into the enteric circulation
by constructing a side-to-side anastomosis between the donor duodenum and the recipient
small bowel or recipient bladder ([Fig. 8]).
Fig. 8 Simultaneous pancreas–kidney transplantation. Yellow arrow indicates transplant artery graft, blue arrow indicates transplant vein graft, and green arrow indicates duodenojejunal anastomosis. PV, portal vein; Tx K, transplanted kidney;
Tx. P, transplanted pancreas.
Vascular Complications of the Transplanted Pancreas
Vascular complications of the transplanted pancreas can be broadly divided into thrombosis,
stenosis, hemorrhage, aneurysms, and AVM.[77]
[78]
Imaging investigations usually start with a Doppler study to determine the presence
of waveform tracings from the implicated vessel. Suspicious duplex US findings should
be evaluated with contrast-enhanced CT or contrast-enhanced magnetic resonance imaging
(MRI); these noninvasive modalities have largely replaced catheter angiography as
means of diagnosis, although the latter remains the gold standard for the assessment
of pancreatic artery complications following transplant.[78] One advantage of catheter angiography is the ability to proceed directly to endovascular
treatment in the same procedure.
Transplant Artery Thrombosis
This is the most severe posttransplantation vascular complication predisposing the
graft to dysfunction and necrosis.[1] It most commonly occurs within the first 3 months following transplantation.
The symptoms of thrombosis include unexplained hyperglycemia, tenderness over the
graft, graft enlargement, and, in bladder-drained grafts, hematuria and decreased
urinary amylase.[6]
Accurate and expedient imaging diagnosis of arterial thrombosis is essential because
early revascularization with or without thrombectomy may salvage the graft[79] ([Figs. 9 ]
[10]).
Fig. 9 Blue arrows point to the site of the proximal occlusion of the upper of the two transplanted
pancreas arteries on (A) coronal maximum intensity projection reformatted CT (computed tomography) and (B) digital subtraction angiography. Revascularization (yellow arrow) was achieved using
2-mm balloon angioplasty.
Fig. 10 A 26-year-old female who underwent pancreatic transplantation 4 months previously
presented with a firm mass in the right iliac fossa. (A) Computed tomographic angiography (B) digital subtraction angiography show right external iliac artery (EIA) occlusion
(green arrow) shortly after Y graft. EIA reforms at the level of the inguinal ligament
(yellow arrow). Note that the pancreatic transplant arterial anastomosis is widely
patent, and so are both branches (blue arrows). This was treated with a prosthetic
vascular graft (not shown).
Predisposing factors include prolonged cold ischemia, prolonged back-table preparation,
graft rejection, pancreatitis, stump thrombi, and vessel trauma.[79]
Complications of pancreas graft thrombosis include graft dysfunction, leakage of pancreatic
secretions, pancreatitis, necrosis, and sepsis. Prompt surgical exploration is often
required.[6]
Transplant Artery Stenosis
Arterial stenosis following pancreas transplantation is less common than arterial
thrombosis and is typically an early posttransplantation complication.[1] Predisposing factors include rejection clamp injury, faulty surgical technique,
catheter-induced trauma, and disruption of the vasa vasorum.[80] This is usually assessed with arterial Doppler, with a peak systolic velocity of
2 m/second or greater being suggestive of an arterial stenosis greater than 50%.[1]
Treatment options for arterial stenosis include angioplasty, covered stent placement
in selected cases, and surgical revascularization.[81] Early treatment with revascularization preserves graft function and often prevents
retransplantation ([Fig. 11]).
Fig. 11 A 31-year-old male who underwent pancreatic and kidney transplant 4 years previously
was admitted with urinary tract infection, sepsis, and right iliac fossa pain. (A) Coronal maximum intensity projection reformatted CT (computed tomography) shows
occluded Y graft (green arrow) and no enhancement of the pancreas. (B, C) The patient underwent angioplasty and stent deployment.
Pancreatic Transplant Hemorrhage
Intra-abdominal bleeding in the early period after pancreas transplantation is typically
associated with systemic anticoagulation initiated to prevent graft thrombosis.[6] However, delayed hemorrhage is typically secondary to pseudoaneurysm rupture.
In common with treatment of other visceral pseudoaneurysms, endovascular embolization
is usually the first line of therapy, offering better morbidity and mortality than
open surgical interventions. A covered stent can be deployed in the common/external
iliac artery to exclude the pseudoaneurysm ([Fig. 12]). Surgical exploration may be necessary when endovascular treatment fails or where
hematoma evacuation is required.[6]
Fig. 12 A 38-year-old female with a previously failed pancreatic transplantation presented
with acute hematuria and deranged clotting. (A) Abdominal CT (computed tomography) suggests active hemorrhage (yellow arrow) from
the right common iliac artery (CIA) into the bladder through the transplanted pancreas’
duodenal pouch (green arrow). (B) Angiography confirms right CIA contrast extravasation. (C) This was treated with a covered stent.
Pancreatic Transplant Vein Thrombosis
Venous thrombosis is the most common cause of early technical pancreatic transplant
failure (70%).[82] Early thrombosis may be associated with acute or hyperacute rejection. However,
the majority (60%) of grafts lost to thrombosis are histopathologically normal.
The etiology is thought to be due to relative stasis caused by compression by a perianastomotic
fluid collection, due to phlebitis related to pancreatitis, or because of the shift
in organ position, leading to stretching or twisting of the venous anastomosis.[83]
Given that pancreas grafts are predisposed to thrombosis, some propose routine postoperative
anticoagulation.[84] Meticulous surgical technique and rigorous avoidance of the transplant organ damage
are considered to be more effective methods to decrease the incidence of early thrombosis.[85]
Endovascular treatments of pancreas transplant venous thrombosis include thrombolysis,
mechanical thrombectomy, and deployment of metal stents for anastomotic stenosis or
kinks ([Fig. 13]).[85]
Fig. 13 A 35-year-old female presented with severe hyperglycemia at day 5 following simultaneous
pancreas–kidney transplantation. (A) Coronal oblique maximum intensity projection reformatted CT (computed tomography)
shows a filling defect within the vein graft in keeping with nonocclusive thrombus
(blue arrow). (B) Catheter venography confirms graft thrombus (yellow arrow). (C) This was treated with mechanical thrombectomy.
Pancreatic Transplant Arteriovenous Fistula Embolization
An arteriovenous fistula (AVF) is most commonly the consequence of biopsy of the transplanted
allograft when the walls of both artery and vein are iatrogenically lacerated.[1] It, however, can be iatrogenic soon after pancreatic transplantation, as in our
case ([Fig. 14]).
Fig. 14 (A) Axial CT (computed tomography) demonstrates an arteriovenous fistula (AVF) in the
transplanted pancreas (yellow arrow). (B) Three-dimensional reconstruction of the AVF. IVC, inferior vena cava.
At duplex US, an AVF is identified as a focal area of aliasing involving a high-velocity
low-resistance feeding artery and a pulsatile “arterialized” draining vein.[86] Dual-phase (arterial and portal venous) CT helps in the characterization and anatomical
localization of these vessels.
AVFs may be associated with regional areas of transient parenchymal enhancement on
contrast-enhanced CT/MRI. Large AVFs may cause graft ischemia and dysfunction due
to arterial “steal” phenomenon.[1] They are usually treated with transarterial embolization.
Nonvascular Interventions on the Transplanted Pancreas
Due to the lack of consistent clinical symptoms or markers for rejection, pancreatic
biopsies have become the standard method in diagnosing transplant rejection. The biopsy
techniques are either through cystoscopy or by percutaneously using US and/or CT guidance,
with a reported success rate of 83%.[87] Cystoscopic biopsies require general anesthesia and only allows biopsy of the pancreatic
head.[88]
No major complications occurred in a series of 42 attempted percutaneous biopsies.[87] However, there is a risk of causing vascular damage to the allograft, including
AV fistulation.[1]
Similar to native pancreas percutaneous interventions, drainage of peripancreatic
transplant collections can be attempted on the transplanted pancreas with US or CT
guidance.
Conclusion
The anatomical location of the pancreas has meant that historically, pancreatic pathologies
were treated by either major surgery or conservative means.
Image-guided percutaneous intervention for a wide range of pancreatic disease is now
routine.
Vascular complications of pancreatic disease benefit from accurate diagnosis with
modern imaging techniques and may require immediate treatment. Endovascular intervention
for the treatment of arterial and venous peripancreatic pathology is demonstrably
effective.
Ablative techniques from cancer are emerging and may help to alleviate the high morbidity
and mortality associated with pancreatic cancer and its treatment.
Vascular complications of the transplanted pancreas can be severe and cause early
technical pancreatic transplantation failure. Percutaneous pancreas transplant biopsy
has a high success rate and is most accurate in diagnosing transplant rejection. Advances
of endovascular interventions permit revascularization and may salvage the graft.
