Keywords
Acute necrotizing pancreatitis - pancreatic fistula - urinary bladder fistula
Introduction
Acute pancreatitis is an important cause of acute abdomen presenting to the emergency
room and has the potential to involve peripancreatic tissues or even remote organs
or organ systems[[1]] due to the digestive enzymes within the PFC. This autodigestive property may result
in fistulization with hollow viscera or to the skin. Other mechanisms of fistula formation
include ischemic necrosis of the viscera owing to vascular thrombosis and iatrogenic
insult. Within the gut, colon and duodenum constitute frequent sites.[[2]] Fistulization to the urinary track has rarely been described; communication with
the urinary bladder has been reported once.[[3]] In the present case, we describe severe acute necrotising pancreatitis in a 28-year-old
chronic alcoholic man that resulted in a fluid collection which tracked down to the
pelvis and spontaneously drained into the urinary bladder via a pancreatico-vesical
fistula.
Case Report
A 28-year-old male, chronic alcoholic, developed severe acute pancreatitis and was
started on conservative therapy at an outside facility. The patient showed mild improvement
in symptoms and took discharge against medical advice after 3 weeks of admission.
Four days later the patient presented at our institution with severe generalized abdominal
pain with marked tenderness over epigastrium and left flank and significant nausea.
The patient was febrile (38.2°C) with a respiratory rate of 24/min. He was normotensive.
Bowel sounds were diminished. His serum amylase and lipase levels were high. CT abdomen
revealed a fatty liver [[Figure 1]] and an enlarged pancreas with non-enhancing areas, peri-pancreatic fat stranding,
and acute fluid collections adjacent to body and tail of the pancreas [[Figures 1] and [2]] extending along the retroperitoneal plane toward the pelvis and resting on the
left superolateral wall of the urinary bladder [arrow in [Figure 2]].
Figure 1: CECT axial section in venous phase depicts fluid collection (C) in the body-tail
region of pancreas. L depicts fatty infiltration of liver, a result of chronic alcoholism
in the current case
Figure 2: CECT coronal reformation in venous phase reveals the fluid collection (C) tracking
down to the pelvis. It lies on the superior wall of the bladder on the left side (arrow)
Three days later, the patient started complaining of burning micturition. The urine
had a brownish tinge, and was turbid in character with a foul smell. Urine microscopy
was devoid of significant bacterial count or casts. An abdominal sonogram revealed
normal kidneys but the UB wall was thickened with thick mobile echoes. Similar echoes
were present in the collection lying superolaterally to the UB on left side. This
collection was better demonstrated on prior contrast enhanced CT. Due to approximation
of the collection to the UB wall, sterile pyuria, and turbid brownish urine, a communication
between the UB and the collection was suspected; hence urine was assayed for amylase
and lipase. Urine lipase and amylase were, respectively, 1499 U/L and 1350 IU/L. To
conclusively demonstrate a fistulous tract between the UB and the collection, CT cystography
was done. It depicted contrast extravasation from the left superolateral wall of the
UB into the perivesical collection ([[Figure 3]] in coronal plane; [[Figure 4B]] through H in axial sections; Video 1 in coronal plane). Besides, there was a fluid–fluid
level seen in the UB suggestive of contrast-debris level (open arrow in “I” of [[Figure 4]]). A diagnosis of pancreatico-vesical fistula was thus established. The collection was percutaneously drained and the pancreatic
duct was subsequently stented to abolish its communication with this retroperitoneal
collection. There was a gradual regression of urinary symptoms with progressively
declining urinary amylase levels. A repeat cystogram performed 12 days later did not
show any leakage of contrast suggestive of spontaneous healing of the fistula. The
patient was subsequently discharged and was counselled for abstinence from alcohol.
He was followed up for 5 months during which period he was symptom free.
Figure 3: CT cystography in MIP (maximum intensity projection) and coronal reformation shows
contrast extravasation into the fluid collection from the left superolateral wall
of the urinary bladder
Figure 4 (A-I): Serial images of CT cystography in axial plane depict contrast extravasation into
the fluid collection (B-H), site of leakage of contrast from the urinary bladder (H)
and contrast -debris level (open arrow in I). The debris in this case was from pancreatic
fluid collection
Discussion
Inappropriate activation of pancreatic proenzymes culminates in an attack of acute
pancreatitis.[[1]] This digestive tendency disintegrates both the pancreatic parenchyma and the peripancreatic
tissues. The latter may lead to arterial pseudoaneurysms, fat necrosis, and bowel
perforation. Activation of various protein factors by pancreatic succus may also lead
to vessel thrombosis and tissue inflammation.[[1]]
Pouring of pancreatic secretions into a space lined by granulation tissue leads to
the formation of a pancreatic fluid collection (pseudocysts or walled-off necrosis)
and are common entities in the setting of pancreatitis. However, spontaneous fistulization
or perforation of PFC is found in only about 3’.[[4]] This fistulization can be seen into the pleura,[[5]] peritoneum,[[5]] gut, or to the skin surface. Refractory ascites ensues if peritoneo-pancreatic
fistula is present and refractory pleural effusion is encountered in the setting of
pleuro-pancreatic fistula. Known instances of fistulization or perforation into surrounding
anatomical structures include cases of communications with the free peritoneal cavity,
stomach, duodenum, colon, portal vein, pleural cavity, through the abdominal wall[[4], [6]] and to the kidney.[[7]]
While instances of pancreatic fistulas to the alimentary tract abound in the literature,
pancreatic fistulas to the urinary tract are rare[[7], [8], [9]] and such fistulas usually communicate with the left kidney. Ting et al. described a spontaneous pancreatico-renal fistula in the setting of hypertriglyceridemia-induced
pancreatitis.[[7]] PFC may even obliterate ureters by causing necrosis, thereby presumably causing
a communication with the lumen.[[10]] However, to the best of our knowledge, spontaneous pancreatico-vesical fistula
has been reported only once.[[3]]
In our case, presence of PFC in close proximity to the UB and high urinary pancreatic
enzymes prompted CT cystography that demonstrated pancreatico-vesical fistula. Cystitis
with urinary lipase and amylase can also be seen in UB drained pancreatic allograft.[[11], [12]] The exocrine pancreatic allograft pours the juice into the UB, and thus, urinary
amylase levels are monitored.[[11]] A fall in amylase level in these patients is not desirable since it indicates acute
graft rejection[[11]]; although in our case the decreasing levels were desirable. The release of necrosum
in the UB in our case functioned as a nature’s way to get rid of the debris to detoxify
the system and achieve homeostasis. The fistula, however, healed spontaneously with
percutaneous drainage of the PFC and stenting of the pancreatic duct.
Our case report identifies a unique fistulization in the context of severe acute pancreatitis
due to enzyme rich PFC and underscores the importance of stenting of main pancreatic
duct to obliterate the fistula and thus accelerate healing.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms.
In the form the patient(s) has/have given his/her/their consent for his/her/their
images and other clinical information to be reported in the journal. The patients
understand that their names and initials will not be published and due efforts will
be made to conceal their identity, but anonymity cannot be guaranteed.
