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Abstracts

days for melena, which revealed diffuse ulcerative esophagitis and gastritis.
Repeat endoscopy after another 7 days for recurrent bleeding revealed a
large gastric clot and resolving gastric injury. He did well until approximately one month post-ingestion when he developed symptoms of gastric
outlet obstruction. Endoscopic exam revealed gastric scarring with marked
pyloric stenosis. Endoscopic balloon dilation was performed with temporary improvement. Recurrent symptoms of gastric outlet obstruction 4
months later led to a gastrojejunostomy for relief of symptoms. A gastrectomy was considered, but at the time of surgery the stomach was too
scarred to make this a viable procedure. After his surgery he has been
asymptomatic for 2 months of follow-up.
Conclusions: Caustic acid ingestion can lead to severe sequelae including
esophageal and pyloric stenosis in a relatively short time. Endoscopy
allows assessment and DPEJ placement for nutritional support. Continued
evolution of pyloric stricturing following concentrated acid ingestion may
occur over several months following caustic ingestion.

792
Pseudomyxoma peritonei presenting as a rectal mass
Jorge Sotelo, M.D.1, Mitchell Chorost, M.D.1, Gerald Fruchter, M.D.1
and Ayse Aytaman, M.D.1*. 1Gastroenterology, VA NY Harbor HCS
Brooklyn Campus, Brooklyn, New York, United States.
Purpose: Pseudomyxoma peritonei (PMP) is characterized by gelatinous
intraperitoneal fluid collections and mucinous implants on the peritoneal
surfaces and omentum which usually is derived from an underlying appendiceal or intestinal mucin secreting adenoma or adenocarcinoma. Typical presentations are increasing abdominal girth, ovarian mass, new onset
inguinal hernia or rarely acute appendicitis. We describe a case of PMP
presenting with a rectal mass simulating a rectal carcinoma.
Case History: The patient is a 69 year old male, who was evaluated 4 years
earlier for right lower quadrant pain and constipation. A computed tomography (CT) scan of the abdomen revealed at that time a right lower quadrant
mass and multiple hepatic lesions suspicious for metastasis. Two CT
guided biopsies of the liver lesions revealed cavernous hemangioma.
Colonoscopy was unremarkable except for a small ulceration at the appendiceal orifice with biopsy showing nonspecific inflammation.
He re-presented with a 3 month history of weight loss, constipation,
increasing abdominal girth and was found to have massive ascites and a
painful, hard and fixed rectal mass. Repeat colonoscopy revealed a submucosal, 5cm rectal mass encroaching upon 50% of the lumen, biopsy was
non-diagnostic; in addition there was a 4mm nodule overlying the appendiceal orifice, biopsy revealing acute and chronic inflammation and villotubular changes. CT scan showed extensive ascites with multiple areas of
enhancement, and an extrinsic rectal mass. Paracentesis revealed well
differentiated, bland and tall columnar cells noted in the background of
mucus lakes, consistent with PMP.
Patient underwent surgery for debulking and to relieve obstructive symptoms. Findings revealed bulky gelatinous masses throughout the peritoneum with omental, pelvic, bilateral subdiaphragmatic caking and near
total extrinsic compression of the recto-sigmoid. Patient underwent transverse loop colostomy and limited debulking. Pathology was consistent with
well differentiated mucinous adenocarcinoma consistent also with PMP.
Conclusions: The treatment of PMP is aggressive debulking via laparotomy and possible use of chemotherapy. Except in patients with high-grade
malignant process where only palliative therapy may be indicated, the
median survival can be increased significantly with early diagnosis and
treatment before large volume of disease leads to bowel entrapment by
tumor.
Conclusion: In the differential diagnosis of rectal obstructing lesions this
rare entity has to be considered. It is important to pay special attention to
lesions found at the level of the appendix.

AJG Vol. 96, No. 9, Suppl., 2001

793
Successful treatment of hepatitis B-associated vasculitis with
lamivudine
Veslav Stecevic1, Martin M. Pevzner2 and Stuart C. Gordon1*.
1
Gastroenterology/Hepatology, William Beaumont Hospital, Royal Oak,
Michigan, United States; and 2Rheumatology, William Beaumont
Hospital, Royal Oak, Michigan, United States.
Purpose: Vasculitis is a potentially serious extrahepatic manifestation of
hepatitis B virus (HBV) infection. The treatment of HBV-associated vasculitis with corticosteroids and immunosuppressive agents may worsen the
hepatic disease. We report a case of HBV-associated leukocytoclastic
vasculitis that responded to oral lamivudine as monotherapy.
Case report: A 59-year-old Caucasian woman with chronic HBV developed biopsy-confirmed leukocytoclastic vasculitis in 1978. She had recurrent flares of vasculitis over 20 years, treated continuously with prednisone,
up to 30 mg/d. On initial evaluation in 1998 she had purpuric skin lesions
about her upper and lower extremities and was on prednisone, 30 mg/d. She
had no hepatosplenomegaly or stigmata of chronic liver disease. Laboratory studies showed normal AST and ALT. HBsAg and anti-HBc were
positive, anti-HBs negative, HBeAg negative, anti-HBe positive, HBV
DNA level of 9.3 pg/mL, anti-HCV negative. She was started on lamivudine 150 mg/d. One month later, quantitative HBV DNA was undetectable,
and her vasculitis flares were less intense. Over the next seven months, the
prednisone was tapered and eventually stopped. Twenty-one months later,
her vasculitic lesions had completely resolved. She remains on oral lamivudine. Her HBV DNA is undetectable. She is still HBsAg and anti-HBe
positive and anti-HBs negative. She has not taken any immunosuppressive
agents for over 3 years.
Conclusions: This case illustrates successful treatment of HBV-associated
vasculitis with lamivudine that allowed the patient to stop high dose
prednisone therapy. Acecdotal case reports suggest that lamivudine may be
used in the treatment of HBV-related polyarteritis nodosa in combination
with immunosuppressive agents, but there are no previous reports of
lamivudine as a single agent in the treatment of vasculitis.

794
Pancreatic stenting as a treatment for pancreatic pseudocyst
Deborah A Streletz, Fernando Ramos, Eric M Osgard and Darren S
Baroni*. 1Medicine, Tripler Army Medical Center, Honolulu, HI,
United States.
Purpose: Often pancreatic duct strictures can be a cause of recurrent
pancreatitis and lead to pseudocyst formation. We present a case of a
patient with a high-grade stricture in the pancreatic head and secondary
pseudocyst, both of which responded to endoscopic dilation and stenting of
the pancreatic duct.
Methods: Our patient is a 40-year-old African American female who
presented in November 2000 with her first documented episode of alcoholic
pancreatitis. A CT scan done at the time revealed diffuse pancreatic
inflammation, a dilated pancreatic duct and a 3 to 4 cm peripancreatic
pseudocyst. Her pancreatitis improved with medical management and she
was eventually discharged. As an outpatient, however, even with discontinuation of alcohol, the patient continued to require daily narcotics for pain
control for several months. She presented with recurrent pancreatitis requiring admission in both December 2000 and January 2001. Repeat CT
scans done during both hospital admissions showed persistent dilation of
the pancreatic duct and continued presence of the pseudocyst. In December
2000 the patient was also diagnosed with a right-sided pancreatic pleural
effusion. Eventually, in January 2001 an ERCP was performed and revealed a single marked stricture in the pancreatic head with upstream
dilation in the uncinate, body and tail of the pancreas. Also noted, just
proximal (upstream) to the pancreatic head stricture, was a side branch that
directly communicated with peripancreatic pseudocyst. Dilation of the
stricture was performed with catheter dilators and a 5 Fr 7cm pancreatic
stent was placed which transversed the stricture.

AJG September, Suppl., 2001

Results: The patient clinical status improved greatly and her chronic
abdominal pain nearly completely resolved after pancreatic duct stenting.
The patient has not had any further episodes of pancreatitis since the ERCP.
A repeat CT scan in March 2001 revealed resolution of peripancreatic
pseudocyst and an otherwise normal appearing pancreas.
Conclusions: To our knowledge, this is one of the first reported cases of
a pancreatic pseudocyst secondary to high-grade pancreatic stricture that
has resolved with dilation and endoscopic stenting.
795
Abdominal compartment syndrome due to a large abdominal cyst
Shams Tabrez, M.D., Salma Tabrez, M.D, Houssam Alkharrat, M.D.,
Anil Nagar, M.D., Visvanathan Muralidharan, M.D., Marguerite Pinto,
M.D., Gustave Davis, M.D. and Ingram Roberts, M.D.*.
1
Gastroenterology, Yale-New Haven Health, Bridgeport Hospital,
Bridgeport, CT.
Purpose: Abdominal compartment syndrome is an acute process and
happens mostly in the immediate post-operative period of abdominal surgeries or secondary to abdominal trauma. Rarely it could be a chronic and
insidious presentation.
Methods: 50-y/o female presented with progressively increasing abdominal girth, accompanied with chest pressure, postural dyspnea, oliguria and
50 lbs weight gain. Past medical history was significant for biventricular
cardiomyopathy with anasarca for 23 years, ejection fraction of 20%,
artrial fibrillation and hypertension. There was no history of any hepatobiliary diseases, pancreatitis, abdominal surgeries of trauma or travel. She
was taking coumadin, metalazone, furosemide, digoxin, and lopressor. She
was morbidly obese. There were no stigmata of chronic liver disease. The
abdomen was huge, distended, non-tender, and dull on percussion with
distant bowel sounds with no palpable organomegaly. The stool was
negative for occult blood. The laboratory values were remarkable for
hemoglobin of 6.0 g %, BUN and creatinine of 101 MG % and 5.5 MG %
respectively (her baseline creatinine 1.11.4), serum albumin 3.2 g/dl and
Prothrombin time 22 sec. Rest of the laboratory results including white cell
count, platelets, liver enzymes, and amylase were normal. An abdominal
Ultrasound revealed grossly enlarged dense fluid filled cyst-Vs-large tense
ascites filling the whole abdominal cavity and compressing the internal
organs, these findings were confirmed by CT scan of abdomen and pelvis.
Diagnostic paracentesis showed a serosanguinous fluid that had 23K RBC,
42 PMN, Amylase 148 IU/L, LDH 2718 IU/L, and SAAG of 0.2, which
was compatible with a non-portal hypertension process. Large Volume
Paracentesis drained a total of 14 L, with tremendous improvement in the
renal function. The working diagnosis was Abdominal Compartment Syndrome secondary to either a large mesenteric, ovarian or pancreatic-pseudo
cyst. Exploratory laparotomy was performed which revealed a large cyst
occupying the whole abdomen, walled by the thick fibrous tissue with
normal reproductive organs. On marsupialization of the cyst a total of 15
L of hemmorhagic fluid was drained. Frozen section of the cyst was
composed of thick fibrous wall with no epithelial and malignant cells. The
findings were most likely compatible with chronically organized hematoma.
Conclusions: This was an unusual case of hematoma, which progressively
got enlarged and organized over a period of time and finally presented with
Abdominal Compartment syndrome.
796
A case of clostridial pancreatitis: a medical nightmare!
Shams Tabrez, M.D., Visvanathan Muralidharan, M.D., Houssam
Alkharrat, M.D., Salma Tabrez, M.D., Anupama Upadaya, M.D., Ofelia
Balta, M.D., Gregory Soloway, M.D., Howard Taubin, M.D.* and
Ingram Roberts, M.D. 1Gastroenterology, Yale-New Haven, Bridgeport
Hospital, Bridgeport, CT.
Purpose: Biliary pancreatitis can be complicated with secondary bacterial
infection. These are frequently polymicrobial ascending from the gut,

Abstracts

S249

including E. Coli, Enterobacter, Klebsiella, and Enterococci. Anaerobes

including Bacteroides and Clostridia has also been reported. Clostridial
pancreatitis has been reported in the literature but usually following some
intervention.
Methods: We are presenting an unusual case of pancreatitis, which presented ordinarily as presumed biliary pancreatitis but had a drastic ending.
An 86 year-old female presented with sudden onset of severe upper
abdominal pain. Her past medical history was remarkable for hypercholesterolemia, TIAs and osteoporotic fractures. Admitting labs showed hemoglobin 14.5 GM %, hematocrit 42.3, WBC 7.3, platelets 174 K, amylase
1541, lipase 15644, AST 451, ALT 122. Ultrasound of the abdomen
showed normal liver, distended gallbladder, and a CBD 9 mm wide with no
evidence of gallstones. CXR showed a left basal effusion with questionable
retrocardiac infiltrate. She was admitted to the regular medical ward with
a presumed diagnosis of gallstone pancreatitis. She was started on intravenous antibiotics, with the plan of performing with ERCP if her condition
deteriorated. The next morning she became increasingly jaundiced, unresponsive and obtunded and was transferred to the intensive care unit. She
was noted to be hypotensive and the blood gases revealed significant
acidosis. An urgent CBC revealed a hematocrit of 6.2. A peripheral blood
smear showed a few histiocytes and scant RBCs. The blood specimen had
a high hemoglobin content with low RBC count and the total bilirubin was
21.3, suggesting massive intravascular hemolysis. Despite aggressive attempts at resuscitation the patient died. An autopsy was carried out which
showed severe Pancreatico-Biliary sepsis as the cause of her death and the
organism was identified as Gram positive rods most likely Clostridium
Perfringens.
Conclusions: Our patient developed spontaneous pancreatitis and ascending cholangitis with severe sepsis and hemolysis. This case illustrates that
clostridial infection, developing into gas gangrene, should be considered
even in non-traumatic in patient with abdominal infection, especially in
cases of biliary pancreatitis associated with ascending cholangitis in elderly
and immunocompromised patients.

797
Gastrointestinal stromal (GIST) leiomyosarcoma arising from the
stomach mimicking as pseudocyst of the pancreas: a challenging
presentation
Shams Tabrez, M.D., Visvanathan Muralidharan, M.D., Salma Tabrez,
M.D., Houssam Alkharrat, M.D., Manoj Jain, M.D., Jeffrey Weiser,
M.D., Scott Weiss, M.D., Gustave Davis, M.D. and Ingram Roberts,
M.D.*. 1Gastroenterology, Yale-New Haven Health, Bridgeport
Hospital, Bridgeport, CT.
Purpose: Adenocarcinoma is responsible for the majority of malignant
gastric neoplasms. Of the non-adenocarcinomatous malignancies, lymphomas are the most frequent. The remaining are predominantly Leiomyosarcomas (LMSs) with an incidence as high as 25% of all non-adenocarcinomatous malignancies. Other rare sarco-mas include rhabdomyosarcoma,
neurofibrosarcoma, fibro-liposarcoma, fibrosarcoma, and hemangiosarcoma.
Methods: A 67 years-old female from Haiti presented in July 1997 with
acute cholecystitis, and underwent Laparoscopic Cholecystectomy. The
intra-operative cholangiogram showed a filling defect in the CBD. The
patient underwent an ERCP. The major ampulla appeared normal; the
Common bile duct (CBD) could not be cannulated after multiple attempts,
yet the bile appeared to flow freely. The Pancreatic duct was normal. Two
weeks later she underwent another ERCP which was again a difficult study.
A precut sphicterotomy was performed and CBD was visualized with no
filling defect. She developed post-ERCP pancreatitis, including pseudocyst formation in the head and near the tail of the pancreas. She had a full
clinical recovery with resolution of the pseudo-cysts at 8 months postpancreatitis. On follow-up 14 months post-pancreatitis she was found to
have moderate rise in Alkaline phosphatase, but she was asymptomatic.
Ultrasonography and CT scan of the abdomen revealed the appearance of
a new cyst at the tail of the pancreas which was considered to be a