AJG September, Suppl.
, 2003
body, most notably on the trunk and upper thighs. The rest of the physical
exam was within normal limits.Upper endoscopy showed non-erosive
gastritis and multiple 23 mm erosions with surrounding erythema in the
mid and distal esophagus. A pinch biopsy of the esophageal lesions resulted
in a 2 x 2 cm sloughing of the mucosa, consistent with an esophageal
Nikolskys sign. There was no bleeding. Pathology revealed a normal
epithelial mucosa.
Conclusion: Esophageal involvement in bullous pemphigoid is rare. The
typical findings of sloughing epithelium and esophageal casts were not
present in this case.We postulate that the classical endoscopic findings of
bullous pemphigoid may not always be present, even though esophageal
involvment is suspected based on clinical presentation. The demonstration
of an esophageal Nikolskys sign via pinch biopsy can be used to confirm
esophageal involvement in the absence of typical findings.
648
SPLENIC HEMATOMA AS A COMPLICATION OF
COLONOSCOPY-A RARE CASE
Yashma Patel, M.D., Lakshmanasamy Somasundaram, M.D.,
Anshuman Jyoti, M.D., Yatin R. Patel, M.D.,
Raman M. Patel, M.D., FACG*. Lancaster, CA.
Splenic injury is an extremely rare complication of colonoscopy yet needs
to be kept in mind to make a timely diagnosis. Review of the literature has
shown that approximately 27 cases have been reported. We present another
case of splenic hematoma resulting from a routine colonoscopy. A 65
year-old Caucasian female with a history of colon polyps presented for a
follow up colonoscopy. The procedure went well and 2 benign polyps were
removed from the sigmoid colon. After the procedure, in the recovery
room, the patient had severe left sided chest pain radiating to the left
shoulder as well as pain on deep inspiration. Complete examination of the
lungs and abdomen was carried out which was perfectly normal. She was
treated with IV Meperidine after which the pain subsided and she was
discharged home on Hydrocodone plus acetaminophen. She presented to
the emergency room that evening because of similar symptoms. She did not
have abdominal pain, nausea, vomiting, fever, chills, or evidence of gas-
trointestinal bleeding. The patient underwent thorough evaluation that
included physical examination, EKG, chest x-ray, x-ray of the left shoulder
and complete blood count all of which were normal. She was advised to
have a CT scan of the abdomen but apparently she was unable to lie flat so
she refused at the time. The patient was discharged to home again on
analgesics and muscle relaxants. Two days later the patient presented for
outpatient follow-up. She was feeling fairly well, but physical exam re-
vealed that there were decreased sounds at the left base and a pleural rub.
There was also moderate tenderness in the left upper quadrant area. At that
time CT scan of the abdomen and pelvis were ordered and showed multiple
layered subcapsular hematoma involving the spleen. The patient was ad-
mitted to the hospital and surgical evaluation was done.Because of the
persistent pain and dropping hematocrit, the patient underwent exploratory
laparotomy and splenectomy. Her postoperative course was unremarkable.
Colonoscopy has become a routine and usually well-tolerated procedure in
the diagnosis of colorectal diseases. Complications of colonoscopy are rare
but can occur. The origin of this patients left sided pain involving the
chest, shoulder, neck, and later the left upper quadrant tenderness, was due
to splenic injury. A high index of suspicion and awareness of all possible
complications is required in order to make a timely diagnosis and prevent
a possibly fatal outcome.
649
ACUTE ON CHRONIC MESENTERIC ISCHEMIA
Yatin R. Patel, M.D., Yashma Patel, M.D.,
Lakshmanasamy Somasundaram, M.D., Anshuman Jyoti, M.D.,
Raman M. Patel, M.D., FACG*. High Desert Gastroenterology,
Lancaster, CA.
Abstracts S215
We present a case of a patient who has chronic mesenteric ischemia
responsible for recurrent abdominal pain, nausea, vomiting, diarrhea, and
weight loss. She then had an acute ischemic episode, which led to this
hospitalization and required surgery. A 74 year-old Caucasian female was
seen in my office on 4/19/99 complaining of recurrent abdominal pain,
nausea, vomiting, and diarrhea for 2 weeks. She has had similar symptoms
for the past 5 years and a 25 lb. weight loss during the previous 2 years. In
1998, she had presented with similar symptoms at which time she had an
EGD, colonoscopy, and small bowel follow thru that were essentially
nonrevealing. On physical examination a mildly cachectic elderly woman
in no apparent distress was seen. Her abdominal examination revealed
tenderness in the right lower quadrant. The rest of the examination was
normal. CBC, chemistry panel, and an ultrasound were all within normal
limits. An EGD done on April 23, 1999 showed moderate erosive gastritis.
At this time her symptoms had continued to worsen with several episodes
of vomiting and diarrhea. On reevaluation she was found to have significant
tenderness in the right lower quadrant with some guarding and bruit in the
midepigastric area. WBC count was now 20,000/mm3. A CT scan showed
thickening of the wall of the cecum and ascending colon. Because of
worsening of symptoms, more significant tenderness and the results of the
CT scan, the patient was hospitalized for further management. The patient
was evaluated by a surgeon and underwent an abdominal aortogram and a
mesenteric angiogram on April 27, 1999, which showed complete obstruc-
tion of the superior mesenteric artery, and 70% narrowing of the celiac axis.
An attempt to do an angioplasty was unsuccessful. Subsequently on 4/30/
99, she had an exploratory laparotomy and underwent a right hemicolec-
tomy with revascularization of both arteries. Histopathology of a section of
the bowel showed ischemic ulceration and edema. Post operatively she did
well. She has been followed till today and I happily report that all of her
G.I. symptoms have resolved and she has gained back 30 lbs. of weight.
The spectrum of ischemic bowel disease comprises of acute and chronic
mesenteric ischemia and colon ischemia and includes arterial as well as
venous disorders. Mortality rates average 71% for the past 70 years.
Diagnosis before intestinal infarction is the single most important factor to
improve these unfortunate results.
650
AMEBIC COLITIS MIMICKING ULCERATIVE PANCOLITIS
Dhanasekaran Ramasamy, M.D., K. Shiva Kumar, M.D.,
Pratheba Chandra, M.D.*. Cleveland Clinic, Cleveland, OH; Mayo
Clinic, Rochester, MN and Center for Digestive Diseases, Union, NJ.
Introduction: Entameba histolytica is distributed throughout the world and
remains a health risk in many countries. Amebiasis is the second leading
cause of death from parasitic disease worldwide. Amebic colitis rarely
presents with contiguous mucosal inflammation mimicking ulcerative pan-
colitis. We present a case of amebic pancolitis that was clinically and
endoscopically indistinguishable from ulcerative colitis (UC).
Case Report: A 57 year-old Indian male presented with a 2-week history
of hematochezia and rectal pain. Physical exam was unremarkable except
for tenderness on rectal exam. Lab studies were unremarkable except for
anemia (Hb 11 gm/dl). Colonoscopy revealed mucosal friability, edema,
erythema with extensive ulceration extending from the rectum to cecum.
He was empirically started on mesalamine for presumed UC, pending
biopsy results. Histology revealed moderately active acute and chronic
inflammation with ulceration and Entameba trophozoites were noted on
PAS staining. He was subsequently treated with metronidazole, resulting in
complete resolution of symptoms.
Discussion: Although most patients infected with E. histolytica are asymp-
tomatic, 4-10% develop invasive disease over a year. Common presenting
symptoms of amebic colitis are bloody diarrhea and abdominal pain.
Complications are fulminant colitis, toxic megacolon, paralytic ileus, per-
foration and obstructive symptoms secondary to amebomas. Invasion of
Entameba through the mucosa and into the submucosal tissues is the
hallmark of amebic colitis. The pathologic spectrum encompasses mucosal
thickening, discrete ulcers, diffusely inflamed and edematous mucosa, and
S216 Abstracts
necrosis and perforation of the intestinal wall. The diagnosis of amebic
colitis rests on the demonstration of E. histolytica in the stool or colonic
mucosa. The mainstay of treatment remains metronidazole, followed by a
luminal agent (paromomycin, iodoquinol, or diloxanide furoate) to eradi-
cate colonization. Amebic colitis rarely presents with continuous mucosal
inflammation, making it indistinguishable from UC. Since the erroneous
diagnosis of UC can lead to disastrous complications, it is imperative to
exclude amebic colitis prior to undertaking steroid therapy, especially in
patients with a prior history of travel to or residence in areas endemic for
E. histolytica. Our case illustrates the need for high index of suspicion in
immigrants and visitors from developing world for amebiasis in the dif-
ferential diagnosis of pancolitis.
651
NEW APPROACH IN THE MANAGEMENT OF PROXIMALLY
MIGRATED STENT WITH AN OBSTRUCTING ANTI-REFLUX
VALVE
Sanjay Nayyar, M.D., Archana Verma, M.D., Benjamin T. Go, M.D.*,
Gonzalo Pandolfi, M.D., Frida Abrahamian, M.D.,
Bashar M. Attar, M.D. Cook County Hospital, Chicago, IL.
Esophageal cancers are usually diagnosed at a late stage requiring palliative
treatment. The use of self-expandable metallic stents (SEMS) have pro-
duced impressive results in improving dysphagia. Even with the increasing
use of SEMS, there are still complications. The most important include
esophageal perforation, hemorrhage, stent migration and fistulization. We
are reporting a case of proximal migration of SEMS with an antireflux
valve (ARV) causing complete occlusion and management. The patient is
a 60 year-old male who was diagnosed 4 weeks prior with an unresectable
squamous carcinoma of the distal esophagus at another hospital. An esoph-
ageal Z-stent with dua ARV was placed. Patient presented to our hospital
2 weeks after placement with inability to handle his secretions. EGD
performed showed the stent located from 20 to 32 cm, with complete
obstruction by the ARV. Attempts to remove the stent were unsuccessful
due to siginificant inflammatory reaction at the proximal end of the stent
but distal to the UES. A needle knife sphincterotome was used to carefully
cut through the ARV to allow the passage of an ERCP catheter into the
stomach. The ARV was then removed by piecemeal fashion with snare
electrocautery to allow deployment of a second SEMS. The tumor extended
from 34 to 41 cm with the GE junction at 40 cm and was dilated with a 12
mm balloon. A 14 cm Z-stent with ARV was deployed through the first
stent with the proximal end at 27 cm and the distal end at 41 cm.
Post-procedure gastrograffin showed ideal stent placement with passage of
contrast into the stomach. Patient was discharged after 2 days without
complications. While most stent migrations occur distally, they can rarely
migrate proximally and be complicated by the ARV. In cases where the
stent cannot be removed endoscopically, removal of the ARV can be done
with a snare electrocautery to allow deployment of a second stent. The
same technique can be utilized with a double channel scope to shorten an
ARV after SEMS deployment.
652
GASTRIC NECROSIS: A COMPLICATION OF GASTRIC
BANDING
Gerald Fruchter, M.D.*, Vlado Simko, M.D., Hatem Shoukeir, M.D.,
Hueldine Webb, M.D., Ayse Aytaman, M.D. VA NY Harbor HCS,
Brooklyn, NY.
Background: Morbid obesity is a growing health problem in the United
States. Patients, who fail conservative measures at weight loss, are potential
candidates for bariatric surgery. Current weight reduction surgery tech-
niques include gastric restriction procedures, gastric bypass, and biliopan-
creatic bypass. We report a rare, potentially lethal, complication of gastric
banding: gastric necrosis necessitating emergent laparotomy and gastrec-
tomy.
AJG Vol. 98, No. 9, Suppl., 2003
Case Report: A 55 year-old male with history of morbid obesity presented
with 5 days of epigastric pain, progressive dysphagia, and vomiting. He had
undergone a laparoscopic gastric banding 7 years prior with subsequent
loss of 150lbs. Upon presentation, the patient was in no distress, weight
187lbs with stable vital signs. Abdominal exam revealed a soft, non-
distended abdomen with mild epigastric tenderness, no guarding or re-
bound with a LUQ subcutaneous reservoir. The WBC was 9.2. CXR and
abdominal films were unremarkable. Esophagogram showed marked con-
striction at the level of the gastric band encircling the fundus with signif-
icant hang-up of barium. On the second day of hospital stay, WBC rose to
29.7; exam was unchanged. An abdominal CT scan was unrevealing except
for a left lung base infiltrate. Antibiotics were initiated. The following day,
patients WBC rose to 35.2 with an unchanged exam. Upper endoscopy
revealed a distended proximal gastric pouch filled with coffee ground liquid
and a large area of confluent ischemia covered by eschar as well as multiple
small islands of ischemia. At surgery, there were multiple areas of necrosis
in the serosal surface of the dilated fundus proximal to the strangulating
ring as well as evidence of peritonitis. The stomach contained over 3 liters
of sloughed gastric lining. A near total gastrectomy with roux-en-y gas-
trojejunostomy was performed. Pathological exam revealed transmural
hemorrhagic necrosis of the fundus with marked thinning and impending
perforation. The patient had an uneventful post-op course.
Discussion: Bariatric surgery is effective in treating morbid obesity. For
gastric banding, revision is occasionally needed to address gastric slippage,
stenosis, as well as stomal obstruction. In our case, gastric banding induced
strangulation with resultant full-thickness gastric necrosis and peritonitis.
Clinicians involved in management of patients who undergo bariatric
surgery need to be aware of the potentially serious consequences inherent
in this form of surgery.
653
SUPRAGLOTTIC LARYNGEAL STENOSIS-A RARE
EXTRAESOPHAGEAL MANIFESTATION OF GERD
Sailaja M. Cheruku, M.D., John OBrien, M.D.*, Carl Malone, M.D.
Southern Illinois University School of Medicine, Springfield, IL.
A 60 year-old caucasian female admitted to hospital for progressive, severe
shortness of breath, over the past 23 weeks. She was sleeping upright in
a chair secondary to orthopnea. She has no history of recent fever or acute
illness. Past medical history included chronic heart burn, hypertension and
obesity. She denied tobacco, alcohol and illicit drug use. She took over the
counter antacids for heart burn. On exam, she had audible inspiratory
stridor and room air oxygen saturation was 80%. An urgent transnasal
fiberoptic laryngoscopy showed inability to visualize true vocal cords and
a large 23 cm mass along the right aryepiglottic fold extending back to
posterior commissure completely obstructing the view of her glottis. The
impression was supraglottic mass obstructing the air way. She underwent
emergency tracheostomy and direct laryngoscopic biopsy of the mass.
Histology showed severe inflammation with granulation tissue and no
evidence of malignancy. Laboratory evaluation of anti nuclear antibody,
anti neutrophil cytoplasmic antibody and angiotensin converting enzyme
levels were normal. Her sedimentation rate was 22. A CT Scan of neck
showed normal appearance of true vocal cords and severe supraglottic
stenosis. In consideration of acid reflux induced ulceration, an upper
endoscopy was performed, which demonstrated a hiatal hernia, normal
esophagus, stomach and duodenum. She was given Pantoprazole twice
daily and discharged home to follow up as out patient, as her post operative
course was uneventful. Ten weeks after treatment with pantoprazole, she
was evaluated with videostroboscopy and fiberoptic nasopharyngolaryn-
goscopy, which demonstrated significant decrease in supraglottic swelling
and inflammation. She denied any episodes of acid reflux. Despite discus-
sions regarding surgery for acid reflux, the patient declined surgery. She is
currently taking once a day pantoprazole. The Plan is to do supraglottic
laryngectomy and removal of tracheostomy tube. Common otolaryngologic
manifestations of GERD include cough, sore throat, hoarseness, laryngitis,
chronic sinusitis, vocal cord nodules, globus, subglottic stenosis and rarely